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PHARMACY PRACTICE-VI

(CLINICAL PHARMACY-II)

Practical Activities
Notebook

Name :
Class :
Class Roll No:
Session :
Academic Year:
Exam Roll No:

Department of Pharmacy, Southern Punjab Institute of


Health Sciences (SPIHS)
LIST OF PRACTICAL ACTIVITIES
ACTIVITY
NAME OF ACTIVITY SIGNATURE
NO.
Introduction to Clinical Pharmacy and Pharmacy Practice
1
(Definitions and Terminologies).
Determination of Body Mass Index (BMI) and Self
2
Monitoring of Blood Glucose (SMBG).
Introduction to WHO Antimicrobial Stewardship (AMS)
3
Program.
A practice to fill up sample AMS review form & pre-
4
authorization/restricted prescribing form.
5 Introduction to WHO AWaRe Groups of Antibiotics.
Introduction to different Essential Medicines lists and
6
comparison between them.
The step-wise approach to conduct ABC/VEN analysis with
7
practice example.
Design a Drug Utilization Review (DUR) and establish DUR
8
criteria of given drugs.
Therapeutic drug monitoring of Digoxin with practice
9
example.
Therapeutic drug monitoring of Theophylline with practice
10
example.
Therapeutic drug monitoring of Gentamycin and
11
Vancomycin with practice example.
Design a Pharmaceutical care plan (SOAP and FARM) for
12
the given case.
13 Clinical Toxicology case studies.
Introduction to various equipment required for intravenous
14
therapy.
Stepwise approach to start IV therapy and calculation of drip
15
flow rate and medication infusion rate.
Introduction to various medication adherence-measuring
16
scales.
Create a table listing all of the medications (Insulin and Non-
17
Insulin) available on the market to treat Diabetes Mellitus.
Design a Pharmaceutical Care Plan for Diabetes Mellitus
18
Patients.
19 Design a Pharmaceutical Care Plan for Tuberculosis Patients

20 Design a Supportive Care Plan for Cancer patients


Introduction to Pharmacoeconomic analysis with practice
21
examples.

ACTIVITY NO 1
DEFINITIONS:-
1. Clinical pharmacy:-
It is defined as set of functions that promote the safe, effective and economic use of medicines for
individual patients. (1)
2. Clinical pharmacy practice:-
It is the discipline of pharmacy which involves in developing the professional role of a pharmacist
(6)
3. Clinical pharmacist:-
Clinical pharmacists are qualified health care professionals that work directly with physicians and
other health professionals, and patients to ensure that the medication prescribed for the patients
contribute to the best possible health outcomes.
4. Rational use of drugs:-
According to WHO in 1986 “Rational use of drugs is defined as a patient receiving medication
appropriate to their clinical needs in doses that meet their own individual requirement for an
adequate period of time and at the lowest cost to them and their community"(2)
5. AMR: Antimicrobial resistance is when Microorganisms such as bacteria, fungi, viruses and
parasites change when exposed to antimicrobial drugs such as antibiotics (antibacterial), antifungals,
antivirals, antimalarial and anthelmintic. As a result, the medicines become ineffective.

6. Irrational prescribing:-
It refers to prescribing that fails to conform to good standards of treatment. It may manifest in
different ways however the end result leads to the irrational use of drugs.
7. Adherence:-
It is an instruction that frequently appears on medicine labels. It suggest that a patient will obey the
doctor’s order without question. (3)
8. Medicine use:-
It is the science and art of restoring or preserving health or due physical conditions by means of
drugs, surgical operations or appliances, or manipulations; often divided into medicine proper,
surgery, and obstetrics.
9. Retrospective study:
This type of study looks backward and examines exposures to suspected risk or protection factors in
relation to an outcome that is established at the start of study.
11. Prospective study:-
A prospective study watches for outcomes, such as development of a disease, during the study period
and relates this to other factors such as suspected risk or protection factors.

12. Essential drugs:-


WHO in 1975 defined essential drugs as “those considered to be of utmost importance and hence
basic, indispensable, and necessary for the health needs of population. They should be available at all
times, in proper dosage forms, to all segments of society"(2)
13. Pharmaceutical equivalents:-
These are the drug products I similar dosage forms and route of administration that contain same
amount of active drug ingredient i.e. same salt or ester of the same therapeutic moiety.
14. Therapeutic equivalents:-
Drugs are said to be therapeutically equivalent only if they are pharmaceutical equivalents and can
be expected to have the same clinical effect and safety profile as one another.
Therapeutic equivalence = bioequivalence + Pharmaceutical equivalence
15. DUE/DUR:-
Drug use evaluation or drug utilization review involves the development, use, monitoring, use
references and adjustment of objective, measurable criteria that describes the appropriate use of a
drug. Or
“DUR is defined as an authorized structure ongoing review of healthcare provider prescribing,
pharmacist dispensing, and patient use of medication.” (6)
16. Prospective DUR:-
Evaluation of patient’s therapy before medication is dispensed.
17. Retrospective DUR:-
Evaluation of patient’s therapy after the patient has received the medication.
18. Concurrent DUR:-
Ongoing monitoring of drug therapy during the course of treatment.
19. ABC analysis:-
ABC Analysis is an integral part of drugs/material management in an inventory. Category A has
products that are most important and have the highest values. It is the smallest category with minimal
products. B: drugs in this category are bigger in terms of volume but less expensive as compared to
A. C; it contains the most items of an inventory and are least expensive.
20. VEN analysis:-
VEN analysis is a method that helps to prioritize for purchasing medicines and keeping stock. The
medicines are categorized according to their health impact that is into vital, essential, and non-
essential.
21. DUR criteria:-
DUR criteria are statements that define correct medicine use and should be strictly followed.
22. DUR threshold:-
A threshold refers to the percentage of charts or records that will meet or exceed the established
criteria for the medicine. DUR threshold is a standard (benchmark) against which treatment criteria
is judged.
23. Intervention:-
The act or fact of taking action about something in order to have an effect on its outcome.
24. Clinical pharmacokinetics:-
It is the application of pharmacokinetic methods to drug therapy in patient care. (5) OR
It is the discipline that describes the absorption, distribution, metabolism, and elimination of drugs in
patients requiring drug therapy.
25. Clearance:-
Clearance is a pharmacokinetic measurement of the volume of plasma from which the drug is
completely removed per unit time. It determines the steady state concentration for a given drug. (8)
26. Creatinine clearance:-
Creatinine clearance (CrCl) is the volume of blood plasma cleared of creatinine per unit time. It is a
rapid and cost-effective method for the measurement of renal function. Both CrCl and GFR can be
measured using the comparative values of creatinine in blood and urine. (9)
27. Volume of distribution:-
It is a proportionality constant that relates the amount of drug in the body to the serum concentration.
It is measured in ml or L. or “It is the hypothetical volume that would be necessary to contain the
total amount of an administered drug at the same concentration that it is observed in the blood
plasma” (9)
28. Half-life:-
It is the time taken by the drug present in the plasma to reduce by its one half of its original quantity.
It can vary from few secs to min to hours and sometimes even days. Different drugs have different
half-lives. (9)
29. Linear pharmacokinetics:-
It obeys dose dependent kinetics. In this pharmacokinetic parameters of a drug will not change with
change in the dose of the drug.
30. Non-linear pharmacokinetics:-
It refers to kinetic processes that results in disproportional changes in plasma drug concentration
when the dose is changed. Clearance is not constant. It changes with the dose.
31. Bioavailability:-
It is the rate and extent by which the drug reaches the systemic circulation after its administration.
The IV bioavailability is always 100%. (9)
32. Steady state concentration:-
It describes the dynamic equilibrium in which drug concentrations consistently stay within the
therapeutic limits for long, potentially indefinite, periods. In this the amount of drug absorbed is
equal to the amount of drug excreted.

33. Therapeutic window/range:


The range between the minimum inhibitory concentration (MIC) and minimum toxic concentration
(MTC) represents a therapeutic window. It is the range of blood level wherein the drug is producing
the desired effect without the feared toxicity.
34. Bioequivalence:
It is the biochemical similarity of two or more drugs that share the same active ingredient and
outcome for the patients.
35. Intrinsic clearance:-
It is the ability of the organ (liver) to remove drug in the absence of flow limitations and binding to
cells or proteins in the blood. Or it is the intrinsic ability of hepatic enzymes to metabolize the drug
which is commonly referred to as intrinsic clearance”. It is discussed with extraction ratio (E). (7)
36. High clearance drugs:-
These drugs are rapidly and extensively cleared from the body by the liver. In this the clearance of
the drug is equal to the blood flow to the organ, these drugs have high extraction ratios. For e.g.
propranolol, verapamil, morphine and lidocaine. (7)
37. Low clearance drugs:-
These drugs are not efficiently cleared by the liver and are extracted less avidly and incompletely
from hepatic blood. In this the clearance of the drug is equal to the fraction of the unbound drug in
the blood and intrinsic ability of the organ to clear unbound drug from the blood. For e.g. warfarin,
theophylline, diazepam. (7)
38. Michaelis-Menten kinetics:-
It tells us that some drugs do not follow linear pharmacokinetics. After increase in dose the enzymes
responsible for metabolism or elimination may start to become saturated, when this occurs, the
maximum rate of metabolism is reached and further no metabolism occurs irrespective of the dose
concentration. This is called as Michaelis-Menten kinetics.
39. Non-linear protein binding:-
It simply means an increase in the fraction of unbound drug with an increase in the total drug
concentration.
40. Pharmacokinetic models:-
These are useful to describe data sets, to predict serum concentrations after several doses or different
routes of administration, and to calculate pharmacokinetic constants such as clearance, volume of
distribution, ad half-life.
41. Pharmaceutical care:-
Pharmaceutical care is a co-operative patient-centered system for achieving specific and positive
patient outcomes from the responsible provision of medicines. The practice of clinical pharmacy is
an essential component in the delivery of pharmaceutical care.(1)

42. DTP:
“Drug therapy problem is defined as any undesirable event experienced by a patient which involves,
or is suspected to involve, drug therapy and that interferes with achieving the desired goals of
therapy” (7)
43. MTM:-
It is defined as a distinct service or group of services that optimize therapeutic outcomes for
individual patients. MTM services are independent of, but can occur in conjunction with, the
provision of medication product. (7)
44. PWDT:-
Pharmacists workup of drug therapy (PWDT) it is a systematic guide to the problem solving process
needed to identify, prevent or resolve a patient’s drug related problem. (7)
45. FARM: It is an alternative approach to document drug therapy and plans. F = Findings, A=
assessment, R= resolution of problem, M=monitoring.
46. SOAP: - It is a documentation format where S= subjective Information, O= objective
information, A=assessment, P= pharmacotherapy care plan.
47. PRIME: - It is a component of pharmacotherapy workup where P= pharmaceutical based
problems, R= risks to patient, I=Interactions, M=mismatch between medications and E= efficacy
issues.
48. CORE: - It is a component of pharmacotherapy workup were C= Condition or potential need,
O=Outcomes desired for the condition, R= regimen and E= evaluation of parameters.
49. Etiology:-
It is the cause, set of causes, or manner of causation of a disease or condition.
50. Epidemiology:-
A branch of medicine which deals with the incidence, distribution, and possible control of diseases
and other factors relating to health.
51. Pathology:
It is concerned with the mechanism of disease process, what the disease does, and how it does so.
52. Clinical presentation:-
The typical pattern of clinical features (including signs and symptoms) caused a disease is called its
clinical presentation.
53. Evidence based medicine (EBM):-
EBM integrates clinical experience and patient values with the best available research information.
It is the conscientious, explicit, judicious, best evidence in making decisions about the care of
individual patients.
54. Clinical toxicology:-
It is a subspecialty of toxicology dealing with the bedside management of poisoned patients,
including definitive toxicological diagnosis, assessment of immediate severity and long term
prognosis, and selection of treatments including antidotes.
55. ADR:-
It is an undesired harmful effect that occurs during treatment with a drug or drug therapy.
56. Side effects:-
Any effect of a drug, chemical, or other medicine that is in addition to its intended effect, especially
an effect that is harmful or unpleasant.
57. Poisoning:-
It refers to an injury or death due to swallowing, inhaling touching or injecting various drugs,
chemicals, venoms or gases. Or any substance that can cause severe organ damage or death if
ingested, breathed n, injected into the body or absorbed through the skin.
58. IV drug therapy:
It is a treatment that infuses intravenous solutions, medications, blood, or blood products directly
into a vein.
59. Isotonic Fluids:
These are IV fluids that have a similar concentration of dissolved particles as blood. In this the
osmolarity is same as the serum osmolarity.
60. Hypertonic fluids:-
It contains higher concentration of solute as compared to plasma and interstitial fluid. It draws fluids
into the extravascular compartment from the cells and the interstitial compartments.
61. Hypotonic fluids:
These have a lower concentration of dissolved solutes than blood. It shifts fluids out of the vascular
compartment, hydrating the cells and interstitial compartments.
62. Crystalloids:-
Crystalloids are water with electrolytes that form a solution that can pass through small permeable
membranes.
63. Colloids:-
Colloids contain solutes in the form of large proteins or other similar sized molecules.
64. Phlebitis:-
It is the inflammation of one or more layer of the vein. Causative factors are classified as
mechanical, chemical, bacterial and post infusion phlebitis.
65. Embolism:-
An embolism is a blocked artery caused by a foreign body such as a blood clot or an air bubble.
66. Extravasation:-
It is the leaking of vesicant drugs into the surrounding tissue. It can cause severe local tissue damage.
67. Infiltration:-
It is the administration/entry of fluid into the surrounding tissue.
68. Compliance:-
Compliance means the extent to which a patient follows instructions issued to him by the medical
personnel. (4)
69. Adherence:-
It is an instruction that frequently appears on medicine labels. It suggest that a patient will obey the
doctor’s order without question. (3)
70. Concordance:-
It is the degree to which the patient and clinician agree about the nature of the illness and the need
for treatment. Simply it relates to the process and outcome of a medical consultation.
71. Stroke:-
It is a cerebrovascular disease, also referred to as brain attack. It is a rapid development of clinical
signs of focal disturbance of cerebral function, lasting for more than 24h or leading to death, with no
apparent cause other than a vascular sign. It is of 2 types, transient ischemic, hemorrhagic.
72. Epilepsy:-
It is a brain disorder which is characterized by the occurrence of repeated seizures. “It is a
paroxysmal event due to abnormal excessive or synchronous neuronal activity in brain.” (11)
73. Status epilepticus:-
It is defined as a single epileptic seizure lasting for more than 5 minutes or two or more seizures
within a 5 minute period without the patient becoming conscious. (11)
74. Meningitis:-
It is the inflammation of the protective membranes covering the brain and spinal cord. A bacterial or
viral infection of the fluid surrounding the brain and spinal cord usually causes the swelling.
75. Tuberculosis:-
“It is a chronic multi-systemic debilitating infection caused by Mycobacterium tuberculosis complex
(M. tuberculosis and M.bovis).” (11)
76. LTBI:-
Latent tuberculosis infection. In this the bacteria can live in your body without making you sick. The
patient is infected but the body is able to fight the bacteria and stop them from growing.
77. Pulmonary T.B:-
In this the bacteria primarily attacks the lungs. Hence the name pulmonary T.B. chest pain,
breathlessness, severe coughing are the major signs.
78. Extra pulmonary T.B:-
It is the T.B infection that occurs in organ system other than lungs. Caseating granulomas, regardless
of location, can spread tubercle bacilli and cause symptoms. Because of muted or altered symptoms,
the diagnosis of TB is difficult and often delayed in immune-compromised hosts.
79. MDR-TB: - Multi drug resistance tuberculosis infection. In this the bacteria are at least resistant
to either isoniazid or rifampin
80. DOT:-
Directly observed therapy refers to a trained health care worker or other designated individual
(excluding a family member) provides the prescribed TB drugs and watches the patient swallow
every dose.
81. UTI: - Urinary tract infection is an infection in any part of your urinary system-your kidneys,
ureters, urethra ad bladder.
82. Malaria fever:-
“It is a blood borne parasitic infection caused by plasmodium species”, people who get malaria are
typically very sick with high fevers, shaking, have chills hence the term malaria fever. (11)
83. Typhoid fever:-
Also known as enteric fever. It is a potentionally fatal multisystemic illness caused primarily by
salmonella typhi.
84. AIDS:-
Acquired immune deficiency syndrome. “It is a progressive state of immunodeficiency induced by
HIV-1 or HIV-2 viruses” (11)
85. HIV:-
Human immune deficiency virus is a virus that attacks the body’s immune system.
86. Anti-retroviral therapy (ART):-
ART is treatment for people infected with human immunodeficiency virus (HIV) using anti-HIV
drugs.
87. Reverse transcription:-
It is a process of synthesizing DNA using RNA as a template and reverse transcriptase as a catalyst.
88. Dengue fever:-
“It is a viral hemorrhagic fever caused by Dengue virus and characterized by fever,
thrombocytopenia, hemorrhagic and capillary leak infestations” (11)
89. Conjunctivitis:-
Also called as pink eye. “It is the inflammation or infection of the transparent membrane that lines
your eyelid and eyeball”
90. Diabetes Mellitus:-
“It is a complex metabolic disorder characterized by hyperglycemia (glucose intolerance) resulting
from relative or absolute deficiency of insulin” (11)
91. Micro-Vascular Complications:-
These are long-term complications that affect small blood vessels. These include retinopathy,
nephropathy and neuropathy.

92. Macro-Vascular complications:-


Diseases of the large blood vessels. These include coronary heart disease, cardiomyopathy,
arrhythmias, cerebrovascular disease and peripheral artery disease.
93. T2DM:-
Type 2 diabetes mellitus is a long-term medical condition in which your body doesn’t use insulin
properly, resulting in unusual blood sugar levels.
94. T1DM:-
Type 1 diabetes mellitus is a condition in which your body destroys insulin-making cells in your
pancreas (beta cells).
95:- LADA:-
Latent autoimmune diabetes in adults is a slow progressing form of autoimmune diabetes.
96. MODY:-
“Maturity onset diabetes of young” is a rare form of diabetes which is different from both type 1 and
type 2 diabetes, and runs strongly in families.
97. GDM:-
Gestational diabetes mellitus is a condition in which a hormone made by the placenta prevents the
Body from using insulin effectively. In this glucose builds up in the blood instead of being absorbed
by the cells.
98. IFG:-
“Impaired fasting glycaemia” is sometimes called pre-diabetes. In this blood glucose levels are raised
but are not high enough to diagnose that person as diabetic.
99. DKA:-
“It is a condition of hyperglycemia, acidosis and ketonemia due to severe insulin deficiency”. Body
doesn’t have enough insulin to allow blood sugar into our cells for use as energy.
100. HbA1c:-
It is your average blood glucose levels for the last 2-3 months. If you have diabetes, an ideal Hb1Ac
level is 48mmol/mol or below. If you’re at a risk of developing type 2 diabetes, your target level
should be below 42mmol/mol.
101. IGT
Impaired glucose tolerance (IGT), IGT is defined by a postprandial BG level between 140 and 199
mg/dL (7.8 and 11.0 mmol/L).
102. OGTT:-
It is an oral glucose tolerance test. It measures the body’s ability to metabolize sugar and clear it
from the blood stream. It is a “two-step” process which includes a 1-hour 50-gram non fasting screen
followed by a 3-hour 100-gram. OGTT for those with a 1-hour screening glucose of greater than or
equal to 140 mg/dL (7.8 mmol/L).

103. SMBG:-
Self monitoring of Blood glucose is a useful tool for patients with diabetes to maintain glycemic
control.
104. Basal insulin:-
It is slow acting type of insulin. People take it between mealtimes and before bedtime to control
blood sugar.
105. Bolus insulin:-
It is a type of insulin that is specifically taken at meal times to keep blood glucose levels under
control following a meal. It is rapidly acting insulin.
106. Insulin
It is a peptide hormone produced by the beta cells of pancreatic islets. It regulates the metabolism of
carbohydrates, fats, protein, by promoting the absorbtion of glucose from the blood into the liver, fat
and skeletal muscle cells. Insulin is the one agent that can be used in all types of DM and has no
specific maximum dose, meaning it can be titrated to suit each individual patient’s needs.
107. Incretin effect:-
A greater insulin stimulatory effect after an oral glucose load than that is caused by an intravenous
glucose infusion.
108. DPP4:-
Dipeptidyl peptidase 4 is a glycoprotein, which serves a binding partner for numerous peptides,
among which are adenosine deaminase and extracellular proteins.
109. Amylin:-
It is an amino acid peptide hormone that is co-secreted with insulin by the pancreatic beta-cells in
response to a nutrient stimuli.
110. GLP-1
Glucagon like peptide 1, prevents the liver from making too much sugar, and helps the pancreas
produce more insulin when needed.
111. MNT:-
Medical nutrition therapy is an evidence based proven method for treating type 2 diabetes and
chronic kidney disease.
112. TZD:-
Thiazolidinedione are insulin sensitizers that act on intracellular metabolic pathways to enhance
insulin action and increase insulin sensitivity in critical tissues.
113. HHS:-
Hyperosmolar hyperglycemic syndrome is a serious complication of diabetes mellitus. HHS occurs
when a person’s BG levels are too high for a long period, leading to severe dehydration. (11)
114. Hypoglycemia:-
“it is a state of low blood glucose in blood which leads to deprivation of energy to tissues” (11)
115, SGLT2-i
It is known as Sodium Glucose Cotransporter-2 inhibitor.
116. Metabolic syndrome:-
It is a cluster of conditions/risk factors that occur together, increasing your risk of heart disease,
stroke and type 2 diabetes.
117. Diabetes insipidus:-
It is an endocrinological disorder that causes an imbalance of fluids in the body. In this the kidney
makes large volumes of urine.
118. Hypothyroidism:-
“It is a constellation of signs and symptoms caused by deficiency of thyroid hormone”. This slows
down the metabolism (11)
119. Hyperthyroidism:-
Hyperthyroidism (overactive thyroid) occurs when your thyroid gland produces too much of
hormone thyroxine.
120. Cancer:-
It is an uncontrolled growth of abnormal cells anywhere n the body. These abnormal cells are termed
as cancer cells, malignant cells or tumor cells.
121. Oncology:-
“It is the branch of medicine that deals with the prevention, diagnosis, and treatment of cancer”
122. MBC:-
Minimum bacterial concentration is the lowest concentration of an anti-bacterial agent required to
kill a bacterium over a fixed, somewhat extended period, such as 18 or 24 hours, under a specific set
of conditions.
123. Breast cancer:-
It is a type of cancer in which cells present in the breast starts to grow and divide uncontrollably. Or
it is a disease characterized by the growth of malignant cells in the mammary glands.
124:- Prostate Cancer:-
Is a type of cancer that is marked by an uncontrolled, malignant growth of cells in the prostate gland
( a gland in the male reproductive system).
125. Lung Cancer:-
Lung cancer is cancer that forms in tissues of the lung, usually in the cells that line the air passages.
It is the leading cause of cancer death in both men and women. There are two main types: small cell
lung cancer and non-small cell lung cancer.
126. AKI:-
Acute kidney injury (AKI) refers to an abrupt decrease in kidney function, resulting in the retention
of urea and other nitrogenous waste products and in the dysregulation of extracellular volume and
Electrolytes.
127. Pre-renal AKI:-
Pre-renal acute kidney injury (AKI) , (which used to be called acute renal failure), occurs when a
sudden reduction in blood flow to the kidney (renal hypo perfusion) causes a loss of kidney function.
In pre-renal acute kidney injury, there is nothing wrong with the kidney itself.
128. Intrinsic AKI:-
Intrinsic or intra-renal acute kidney injury (AKI) , which used to be called acute renal failure, occurs
when direct damage to the kidneys causes a sudden loss in kidney function. The treatment of
intrinsic acute kidney injury includes identifying and correcting the cause of the kidney injury.
129. Post-renal AKI:-
Post renal acute kidney injury, which used to be called acute renal failure, occurs when an
obstruction in the urinary tract below the kidneys causes waste to build up in the kidneys.
130. Oliguria:-
Oliguria is the medical term for low urine output.
131. Anuria:-
Anuria, sometimes called enuresis, refers to the lack of urine production. This can happen as a result
of conditions like shock, severe blood loss and failure of your heart or kidney.
132. RRT:-
Renal replacement therapy RRT is therapy that replaces the normal blood-filtering function of the
kidneys. It is used when the kidneys are not working well.
133. GFR:-
GFR stands for glomerular filtration rate. GFR is a measure of how well your kidneys filter Blood. It
estimates how much blood passes through the glomeruli each minute.
134:-Chronic kidney disease (CKD):-
Means your kidneys are damaged and cant filter blood the way they should. The disease is called
"chronic" because the damage to your kidneys happens slowly over a long period of time.
135. EPO:-
Erythropoietin EPO, also known as erythropoietin, hematopoietic, or hemopoietin, is a glycoprotein
cytokine secreted mainly by the kidneys in response to cellular hypoxia; it stimulates red blood cell
production in the bone marrow.
136. Nephrotic syndrome:-
Nephrotic syndrome is a primary glomerular disease characterized by proteinuria,
hyperalbuminemia, hypercholesterolemia, hypoprotenic edema and hyperlipidemia. Because of gross
proteinuria serum albumin is low (<2.5g/dl)
137. Anemia:-
Anemia is a condition in which the number of red blood cells or the hemoglobin concentration within
them is lower than normal.

138. Erythropoiesis:-
Erythropoises production of red blood cells from mature stem cells.
139. Megaloblastic Anemia:-
Megaloblastic anemia is a type of anemia characterized by very large red blood cells.
140. ACD:-
Anemia of chronic disease (ACD) is anemia that is found in people with certain long-term (chronic)
medical conditions that involve inflammation.
141. Pernicious Anemia:-
Pernicious anemia is a type of vitamin B12 deficiency anemia, a disease in which not enough red
blood cells are produced due to the malabsorption of vitamin B12.
142. IDA:-
Iron deficiency anemia ICD happens when there is not enough iron in the body to make red blood
cells. A condition in which blood lacks adequate healthy red blood cells.
143. Pharmaco-economics:-
The process of identifying, measuring, and comparing the costs, risks, and benefits of programs,
services, or therapies and determining which alternative produces the best health outcome for the
resource invested.
144. CMA:-
It involves the determination of the least costly alternative when comparing two or more treatment
alternatives. In this costs can be measured in competing monetary units (euros).
145. CEA:-
Cost effective analysis compares cost of an intervention to its effectiveness measured in natural
health units.
 Costs: Monetary units
 Consequences: Natural units (years of life saved, causes prevented).
146. CBA:-
It is the method that allows for the identification of measurement, and comparison of the benefits
and costs of a program or treatment alternative.
147. CUA:-
Cost utility analysis (CUA) is an economic analysis in which the incremental cost of a program from
a particular point of view is compared to the incremental health improvement expressed in the unit of
quality adjusted life years (QALYs).
148. ICERs
The incremental cost-effectiveness ratio. ICER is a statistic used in cost-effectiveness analysis to
summarize the cost-effectiveness of a health care intervention. It is defined by the difference in cost
between two possible interventions, divided by the difference in their effect.
ICER= C a – C b ÷ E a – E b

149. QALYs
QALY stands for Quality Adjusted Life Year. The QALY is commonly used in health economic
evaluations as a means of quantifying the health effect of a medical intervention.
150. DALYs
Disability-adjusted life year is a measure of overall disease burden, expressed as the number of years
lost due to ill-health, disability or early death.

REFERENCES:-
1. Roger Walker, Clinical Pharmacy and Therapeutics, edited by Cate Whittlesea, Karen
Hodsen, 6th edition, Sep 2019, Page 1-2.
2. Basavaraj K Nanjwade, Jigar M.Patel, Clinical Pharmacy and Therapeutics, Dec 2018,
page 225-226.
3. Oxford Handbook of Clinical Pharmacy, edited by Philip Wiffen, M.Mitchell M.Snelling,
Nicola Stoner, Jan 2012, page 2.
4. Dr B.B Gaitonde, Basic and Clinical Pharmacology and Therapeutics, Page 8.
5. Leon Shargel, Applied Biopharmaceutics and Pharmacokinetics, 7rh Edition, page 5,11.
6. D.Sudheer Kumar, J Krish Naveni, P Manjula, Fundamentals of Clinical Pharmacy
practise, Page 2,117.
7. Joseph T.Dipirio, Pharmacotherapy: A pathophysiologic approach
8. Marie A. Terry L, Kelly, Pharmacotherapy principles and practise, 5th edition.
9. Philip J. Breen, Sunil S. jambhekar, Basic Pharmacokinetic, published in 2009.
10. Karen Whale, Lippincott Illustrated reviews: Pharacology, published in 2014.

ACTIVITY NO 2
DETERMINATION OF BLOOD GLUCOSE CONCENTRATION AND BODY
MASS INDEX (BMI).

APPARATUS:-
• Stadiometer
• Glucometer
• Spirit swab
• Blood lancet
THEORETICAL BACKGROUND:-
1. BMI:-
Body mass index is a value derived from the mass and height of a person. The BMI is defined as the
body mass divided by the square of the body height, and is expressed in units of kg/m², resulting
from mass in kilograms and height in meters.

NORMAL RANGES OF BMI:-

• Underweight: BMI is less than 18.5 kg/m2

• Normal weight: BMI is 18.5 to 24.9kg/m2

• Overweight: BMI is 25 to 29.9kg/m2

• Obese: BMI is 30 kg/m2 or more.

FORMULAS TO CALCULATE BMI:-

• Weight (lb) / [height (in)]2 x 703.


• Weight (kg) / [height (m)]2.
• [Weight (kg) / height (cm) / height (cm)] x 10,000.
2. GLUCOMETER:-
A glucose meter, also referred to as a "glucometer", is a medical device for determining the
approximate concentration of glucose in the blood.

BLOOD GLUCOSE RANGES:-

• Normal Glucose level: between 70 mg/dL (3.9 mmol/L) and 100 mg/dL (5.6 mmol/L).

• Life style modifications required: when between 100 to 125 mg/dL (5.6 to 6.9 mmol/L).
• If fasting blood glucose is 126 mg/dL (7 mmol/L) or higher on two separate tests, diabetes
is diagnosed.

• low fasting blood glucose concentration (hypoglycemia) – below 70 mg/dL (3.9 mmol/L)

• Increased fasting blood glucose concentration (hyperglycemia) is an indicator of a higher


risk to diabetes. 

TYPES OF GLUCOMETER:-

There are two types of glucose meters

1. Standard

2. Continuous.

1. STANDARD GLUCOSE METERS:

These types of meters measure current blood glucose by using a finger stick blood sample placed
on a test strip and inserted into the device.

2. CONTINOUS GLUCOSE METERS/MONITORS:

Continuous glucose monitors (CGMs) work by wearing a sensor placed under the skin that
measures glucose levels in real time. People who might benefit from a CGM include those with type
1 diabetes, people who require tight blood sugar control or don’t experience warning signs of low
blood glucose and those who have frequent high or low levels.

TEST STRIPS:-

Blood glucose test strips (diabetes test strips) are a key component of blood glucose testing. For
some models, it is a plastic test strip with a small spot impregnated with glucose oxidase and other
components. Each strip can be used only once and then discarded. Instead of strips, some models
use discs, drums, or cartridges that contain the consumable material for multiple tests.

HOW DO TEST STRIPS WORK?

On placing a blood drop onto the test strip, the blood sample start reacting with a chemical called
glucose oxidase and produce gluconic acid from the glucose in the blood. The meter transfers a
current to the test strip, at the other end of the test strip this process takes place. The test strip has
electric terminals that allow the meter to measure the current between the terminals. The level of
gluconic acid is responsible for the current produced between the terminals. The blood glucose
meter then uses an algorithm to work out the blood glucose level based upon the difference in
current. Some blood glucose test strips allow the reapplication of more blood to the same test strip
if needed during the test.

STANDARD GLUCOMETER CONTINOUS GLUCOMETER

PROCEDURE:-
A. METHOD TO CALCULATE BMI:

• Remove shoes, hats and bulky clothing if any.

• Undo hairstyles and remove any hair accessories that may interfere with the measurement.

• Ask the individual to stand against the stadiometer with heels together, legs straight and
shoulder relaxed.

• Measure the nearest 0.1cm and record.

• Measure weight as well.

• Calculate BMI using BMI calculator or by applying the formula.

B. METHOD TO MEASURE BLOOD GLUCOSE:

1. First, set out your glucometer, a test strip, a lancet, and alcohol pad

2. Wash your hands to prevent infection. If you are not by a sink, it's okay to just use the alcohol
swab. If you are by a sink and wash your hands thoroughly, you do not have to use an alcohol
swab. 

3. Turn on the glucometer and place a test strip in the machine when the machine is ready.
Watch the indicator for placing the blood on the strip.
4. Make sure your hand is dry and wipe the area you've selected with an alcohol prep pad and
wait until the alcohol evaporates.

5. Pierce your fingertip on the side of your finger, between the bottom of your fingernail to the
tip of your nail (avoid the pads as this can pinch more). 

6. Place the drop of blood on or at the side of the strip.

7. The glucometer will take a few moments to calculate the blood sugar reading.

8. You may use the alcohol prep pad to blot the site where you drew the blood if it is still
bleeding

9. In the end record your readings and interpret it.

OBSERVATIONS:-

• Name: Warda Irfan

• Height: 5ft 3inches

• Weight: 53kg (114.64lb)

• BMI: 20.3 kg/m2

• Blood Glucose level:-97mg/dl

PRECAUTIONS:-

 Make sure to wash and dry your hands before testing.


 Do not squeeze your finger when taking a blood drop sample.
 Apply the correct amount of blood to the test strip. The instructions for use will tell you the
correct amount.
 Pay attention to any error codes that your blood glucose meter may show on the display
window.
 Don’t use different meters from different manufacturers at the same time. Different brands
may give different results.
 Use only the test strips listed by the manufacturer for your device. Don’t use test strips from
a different manufacturer even if they fit your meter because they won’t work.
 Every time you start to use a new box of test strips, make sure to calibrate your meter and
check the strips are within their expiry date. You will find the expiry date printed on the
container.
 Make sure that the lid of your test strips is sealed tightly, as moisture from the air may
affect the accuracy of the result.
 Never share a lancet or a lancing device with anyone.
 Always use a new, sterile lancet (lancets are for single use only).
 Keep your meter and lancing device clean.
 It is essential to discard the used lancet carefully after each use to avoid unintended lancet
stick injuries.

RESULT:-
My BMI is 20.3 kg/m 2 which is in normal range. Also, my blood glucose concentration is 97mg/dl
which lies in normal range as well.

ACTIVITY NO: 3
ANTIMICROBIAL STEWARDSHIP PROGRAM (AMS
PROGRAMME).

DEFINITIONS:-

1. Antimicrobial stewardship program (AMS program):

An organizational or system-wide health-care strategy to promote appropriate use of antimicrobials


through the implementation of evidence-based interventions.

2. Antimicrobial stewardship (AMS):

A coherent set of actions which promote the responsible use of antimicrobials. This definition can be
applied to actions at the individual level as well as the national and global level, and across human
health, animal health and the environment.

3. Antimicrobial resistance (AMR):

Microorganisms such as bacteria, fungi, viruses and parasites change when exposed to antimicrobial
drugs such as antibiotics (antibacterial), antifungals, antivirals, antimalarial and anthelmintic. As a
result, the medicines become ineffective.

4. Empirical antibiotic treatment:

Initial antibiotic treatment targeted at the most probable causative microorganism. The
recommendations should be based on local susceptibility data, available scientific evidence or expert
opinion, when evidence is lacking.

5. Multidrug-resistant bacteria:

Bacteria that are resistant to at least one agent in three or more antibiotic categories.

6. Extensively drug-resistant (XDR):-

It is non-susceptibility to at least one agent in all but two or fewer antibiotic categories (i.e. bacterial
isolates remain susceptible to only one or two categories),

7. Pan drug-resistant (PDR):-

It is non-susceptibility to all agents in all antibiotic categories.


OBJECTIVES FOR THE IMPROVEMENT OF AMS PROGRAMME:
The Global Action Plan on AMR sets out five strategic objectives as a blueprint for countries in
developing national action plans (NAPs) on AMR:
 Objective 1: Improve awareness and understanding of AMR through effective
communication, education and training.
 Objective 2: Strengthen the knowledge and evidence base through surveillance and research.
 Objective 3: Reduce the incidence of infection through effective sanitation, hygiene and
infection prevention measures.
 Objective 4: Optimize the use of antimicrobial medicines in human and animal health.
 Objective 5: Develop the economic case for sustainable investment that takes account of the
needs of all countries, and increase investment in new medicines, diagnostic tools, vaccines
and other interventions
KEY STEPS IN ESTABLISHING A NATIONAL AMS PROGRAMME TO ENABLE
FACILITY AMS
Audience: Ministry and/or department/s responsible for delivering quality-assured medical care and
access to and rational use of medicines
1. Establish a governance structure – e.g. a national AMS technical working group (TWG) linked to
the national AMR steering committee.
2. Review and prioritize the national core elements:

 Identify what is already in place and the level of implementation required.


 Identify the short- and medium/long-term priority core elements.Identify the resources
required.
3. Identify pilot health-care facilities (public and private) for initial AMS rollout:

 Tertiary teaching facilities;


 Regional/state and/or district facilities; and
 Primary care and/or community
4. Develop a national AMS strategy based on indicators.
5. Dedicate financial and human resources as required.
6. Monitor and evaluate implementation of the national AMS strategy.
7. Facilitate access to and/or support pre- and in-service training on optimized antibiotic prescribing.
KEY STEPS TO ESTABLISHING A HEALTH-CARE FACILITY AMS PROGRAMME
Audience: health-care facility leadership, AMS committee and/or AMS team

1. Undertake a facility AMS situational


2. Establish a sustainable AMS governance structure based on existing structures.

3. Prioritize the health-care facility core elements based on the situational analysis:

4. Identify AMS interventions starting with the low-hanging fruit:

5. Develop a health-care facility AMS action plan that specifies the human and financial resources
required.

6. Implement AMS interventions.

7. Monitor and evaluate AMS interventions.

8. Offer basic and continued educational resources and training on optimized antibiotic prescribing.

CHECKLIST OF ESSENTIAL NATIONAL CORE ELEMENTS FOR AMS PROGRAMMES


IN LOW MIDDLE INCOME COUNTRIES (LMICS) – BASIC (LIGHT GREY) AND
ADVANCED (DARK GREY) CORE ELEMENTS

NATIONAL CORE ELEMENTS Yes No

1. National action plan on AMR that states AMS is a priority □ □


□ □
1. NATIONAL PLAN

2. Dedicated funding for the national action plan on AMR


AND STRATEGIY

3. Technical working group on AMS established with clear terms of reference □ □

4. National AMS implementation plan or policy endorsement □ □


5. Monitoring and evaluation mechanism in place for the national action plan on AMR
□ □
6. Integration of the AWaRe classification of antibiotics in the national EML and formulary
□ □
2. REGULATIONS & GUIDELINES.

7. Up-to-date clinical guidelines that include AMS principles and integrate the AWaRe classification of
□ □
antibiotics

8. Regulations on fixed-dose combinations of antibiotics □ □


9a. Regulations on prescription-only sale of antibiotics □ □
9b. Regulation and enforcement of prescription-only dispensing of antibiotics
□ □
10. Measures in place to ensure continued availability of quality-assured antibiotics
□ □
11. Measures in place to ensure affordability of essential antibiotics
□ □
12. Regular public antibiotic awareness campaigns □ □
3. AWARENESS, TRAINING
AND EDUCATION

13. Education in schools on basic infection principles □ □


14. Training on AMS competencies for AMS team members □ □
15. Education and training for all health-care professionals on AMS
□ □
16. Incentives to support implementation of AMS programs in all health-care facilities, including staffing
□ □
standards, training and accreditation

17. National surveillance system on AMC in place. □ □


TECHNOLOGIES
4. SUPPORTING

18. National surveillance system on AMR in place with laboratory capacity to guide optimal use
AND DATA

of antibiotics in clinical practice and update clinical guidelines □ □


19. Diagnostic tests available and capacity building undertaken to optimize antibiotic use.
□ □

CHECKLIST OF ESSENTIAL HEALTH-CARE FACILITY CORE ELEMENTS FOR AMS


PROGRAMMES IN LMICS. BASIC (LIGHT GREY) AND ADVANCED (DARK GREY)
CORE ELEMENTS

Yes No
HEALTH-CARE FACILITY CORE ELEMENTS

1. AMS identified as a priority for health-care facility management


1.LEADERSHI
COMMITMET

2. Health-care facility AMS action plan endorsed that prioritizes activities and measures
progress and accountability

3. Dedicated financial support for the health-care facility AMS action plan

4. Multidisciplinary AMS leadership committee in place with clear terms of reference


2. ACCOUNTABILITY AND

5. Dedicated AMS leader/champion identified for the health-care facility


RESPONSIBILITIES

6. Multidisciplinary AMS team with terms of reference

7. Other health professionals identified and involved in AMS activities

8. Clearly defined collaboration between the AMS and IPC programmes

9a. Regular (descriptive) activity reports on the implementation of the AMS programme

9b. Regular activity reports (status and outcomes) on the implementation of the AMS programme
10. Up-to-date standard treatment guidelines

11. Regular AMS team review/audit of specified antibiotic therapy or clinical conditions at the
health-care facility

12. Advice/feedback from AMS team members is easily accessible/available to all prescribers
13. The AMS team conducts regular ward rounds and other AMS interventions in select health-care
3. AMS ACTIONS

facility departments
14a. Health-care facility formulary with a list of approved antibiotics

14b. Health-care facility formulary with a list of restricted antibiotics

15. Laboratory and imaging services accessible to support AMS interventions

16. Health-care facility access to IT services to support AMS activities

17a. Standardized facility prescription chart and medical records

17b. Health-care facility policy for documenting prescribed medicines


5. MONITORING AND 4.EDUCATION AND

18. Basic training in optimal antibiotic use for health-care professionals

19. Continued training in optimal antibiotic use for health-care professionals


TRAINING

20. Initial and regular training of the AMS team in infection management

21. Monitoring appropriateness of antibiotic use at the unit and/or facility-wide level through audits
MONITORING AND

or PPSsi
SURVEILLANCE.

SURVEILLANCE

22. Monitoring quantity and types of antibiotic use (purchased/prescribed/dispensed) at the unit
and/or facility- wide Level

23. Monitoring of antibiotic susceptibility and resistance rates for a range of key indicator bacteria

24. Monitoring compliance of AMS interventions by the AMS committee

25. Regular evaluation and sharing of health-care facility data on antibiotic use with prescribers
6.REPORTG AND
FEEDBACK

26. Regular evaluation and sharing of health-care facility resistance rates with prescribers

27. Evaluation of appropriateness of data on antibiotic use is shared with prescribers

28. Health-care facility antibiogram for key antibiotics informed by data on antibiotic use and
resistance
OVERVIEW OF THE WHO AWaRe GROUPS AND ESSENTIAL ANTIBIOTICS ON THE
WHO EML50
PERFORMING AMS INTERVENTIONS IN A HEA LTH-CARE FACILITY

Nine common areas for improving antibiotic prescribing:-

PRESCRIPTIONS WHAT TO IMPROVE

1. Overprescribing Antibiotics are prescribed when not needed, e.g. fever without evidence of infection,

asymptomatic urinary tract colonization, viral infections, malaria,

Inflammatory conditions.

2. Overly broad More broad-spectrum antibiotics (WATCH and RESERVE antibiotics) are prescribed than

spectrum are necessary (e.g. surgical prophylaxis).

3. Unnecessary combination Multiple antibiotics are used, particularly with overlapping spectra and in combinations

therapy, including certain fixed- that have not been shown to improve clinical outcomes.

dose

Combinations

4. Wrong antibiotic choice Wrong antibiotic(s) are prescribed for particular indications/infections.

5. Wrong dose Antibiotics are prescribed with the wrong dose (over- or under dosing).

6. Wrong dose interval Antibiotics are prescribed with the wrong dose interval (too much time between doses).

7. Wrong route Antibiotics are prescribed by the wrong route (e.g. IV instead of oral).

8. Wrong duration Duration of antibiotic treatment should be optimized (e.g. antibiotics prescribed for too

long a period, prolonged surgical prophylaxis).

9. Delayed administration Administration of the antibiotic(s) is delayed from the time of prescription. Repeat doses

are not administered in a timely way, which is critical in the case

of septic shock and other serious infections.


APPROPRIATE ANTIBIOTIC TREATMENT-INDICATION AND PRESCRIBE, REVIEW AND STOP
TREATENT.

APPROPRIATE ANTIBIOTIC SURGICAL PROPHYLAXIS-INDICAION, AND PRESCRIBE AND STOP


PROPHY
ACTIVITY NO 4
A PRACTICE TO FILL UP SAMPLE AMS REVIEW FORM AND PRE-
AUTHORIZATION/RESTRICTED PPRESCRIBING FORM.
SAMPLE AMS REVIEW FORM
Patient information
Date:25/3/2021 Department: Surgery Ward: surgical ward: 9
Patient name: Ghulam Fareed Age: 55Y Sex: Male ☐ or Female ☐

Antibiotic prescriptions
Antibiotics prescribed Dose Route Interval Start date
1. Moxifloxacin 400mg IV Every 24h 26/3/2021
2. Linezolid 600mg IV Every 12 h 26/3/2021

Indication for antibiotic treatment


Prophylaxis ☐ Urinary tract Pneumonia ☐ Gastrointestinal Bloodstream
infection ☐ infection ☐ infection ☐
CNS ☐ Skin infection ☐ Bone infection ☐ Other:

Initial review of antibiotic treatment


Is indication for antibiotic Is antibiotic treatment prescribed Comments
treatment documented? according to guideline?
Yes ☐ Yes ☐
No ☐ No ☐ Why not? Comment
Correct dose? Appropriate Treatment duration or review date
Yes ☐ route? Yes ☐ stated? Yes ☐
No ☐ No ☐ No ☐

48-‐hour review of antibiotic treatment


Is antibiotic treatment reviewed? Yes ☐ No If yes, what action?

Escalate ☐ Continue ☐ De-‐escalate ☐ Stop ☐ IV-‐oral switch ☐
Why is antibiotic treatment being continued?
Continuing clinical signs of Confirmed infection ☐ Other (comment):
infection ☐
Microbiology specimens collected? Microbiology results Microbiology results acted upon?
received?
☐ Date: ☐ Comment:
☐ Date:

General comments:
PRE-AUTHORIZATION/RESTRICTED PRESCRIBING FORM

Patient information
Patient name: Mehboob Ahmed Department: Medicine Ward: Medical Ward 12
Age: 22Y Sex: Male ☐ Female ☐ Allergies: Not significant

Indication for Antibiotic treatment


Meningoencephalitis

Request for pre-authorized/restricted antibiotics


Dose and Administration
Antibiotic(s) requested duration route Interval Reason for request
1. Vancomycin 1g IV B.D CNS infection

Are microbiology test results with sensitivity testing available? Yes ☐ No ☐


If yes, provide details:
Date Specimen Pathogen identified and susceptibility results
18/3/2021 CSF fluid taken by LP -

Has the patient already received antibiotic(s)? Yes ☐ No ☐ If yes, what?


Dose and Administration Why is the treatment
Antibiotic(s) prescribed duration route Interval not adequate?
1. Ceftriaxone 2g IV B.D Worsening signs of
infection
Metronidazole 500mg IV TDS Worsening signs and
symptoms.

Requesting physician’s name/contact number: _____________________________________

Comments from the AMS team/Drug and therapeutics committee/Pharmacy department

Approver

☐ APPROVED ☐ NOT APPROVED


Remarks:
Name/signature of specialist:-------------------- Date:--------------------------------------
ACTIVITY NO 5
WHO Model List of Essential Medicines – 22nd List (2021)
Access group antibiotics
Access group Indications
Antibiotics FIRST CHOICE SECOND CHOICE
AMIKACIN − High-risk febrile neutropenia − Sepsis in neonates and
− Pyelonephritis or prostatitis children
(severe)
AMOXICILLIN − Community acquired pneumonia − Acute bacterial meningitis
(mild to moderate)
− Community acquired pneumonia
(severe)
− Complicated severe acute
malnutrition
− Exacerbations of COPD
− Otitis media
− Pharyngitis
− Progressive apical dental abscess
− Sepsis in neonates and children
− Sinusitis
− Uncomplicated severe acute
malnutrition
AMOXICILLIN + CLAVULANIC − Community acquired pneumonia − Bone and joint infections
ACID (severe) − Community-acquired
− Complicated intraabdominal pneumonia (mild to moderate)
infections (mild to moderate − Community acquired
− Exacerbations of COPD pneumonia (severe)
− Hospital acquired pneumonia − Otitis media
− Low-risk febrile neutropenia − Surgical prophylaxis
− Lower urinary tract infections
− Sinusitis
− Skin and soft tissue infections
AMPICILLIN − Community acquired pneumonia − Acute bacterial meningitis
(severe)
− Complicated intraabdominal
infections
− Complicated severe acute
malnutrition
− Sepsis in neonates and children
BENZATHINE − Syphilis
BENZYLPENICILLIN
BENZYLPENICILLIN − Community acquired pneumonia − Acute bacterial meningitis
(severe)
− Complicated severe acute
malnutrition
− Sepsis in neonates and children –
Syphilis
CEFALEXIN − Skin and soft tissue infections − Exacerbations of COPD
– Pharyngitis
CEFAZOLIN − Surgical prophylaxis −Bone and joint infections
CHLORAMPHENICOL − Acute bacterial meningitis
CLINDAMYCIN − Necrotizing fasciitis − Bone and joint infections
CLOXACILLIN* −Bone and joint infections − Sepsis in neonates and
− Skin and soft tissue infections children
DOXYCYCLINE − Cholera − Cholera
− Sexually transmitted infection due − Community acquired
to Chlamydia trachomatis pneumonia (mild to moderate)
− Exacerbations of COPD
GENTAMICIN − Acute bacterial meningitis in −Gonorrhoea
neonates − Surgical prophylaxis
− Community acquired pneumonia
(severe)
− Complicated intraabdominal
infections
− Complicated severe acute
malnutrition
− Sepsis in neonates and children
METRONIDAZOLE − C. difficile infection − Complicated intraabdominal
−Complicated intraabdominal infections (mild to moderate)
infections (mild to moderate)
− Complicated intrabdominal
infections (severe)
− Necrotizing fasciitis
− Surgical prophylaxis
− Trichomoniasis
NITROFURANTOIN − Lower urinary tract infections
PHENOXYMETHYLPENICILLI − Community acquired pneumonia
N (mild to moderate) − Pharyngitis −
Progressive apical dental abscess
PROCAINE Syphilis (congenital) − Syphilis
BENZYLPENICILLIN*
SPECTINOMYCIN − Gonorrhoea
SULFAMETHOXAZOLE + − Lower urinary tract infections − Acute invasive diarrhoea /
TRIMETHOPRIM bacterial dysentery
TRIMETHOPRIM − Lower urinary tract infections

Watch group antibiotics


Watch group Indications
antibiotics First choice Second choice
AZITHROMYCIN − Cholera − Acute invasive bacterial
− Enteric fever diarrhoea / dysentery
− Gonorrhoea – Gonorrhoea
− Sexually transmitted infection due
to Chlamydia trachomatis
− Trachoma
− Yaws
CEFIXIME − Acute invasive bacterial
diarrhoea / dysentery
– Gonorrhoea
CEFOTAXIME* − Acute bacterial meningitis − Bone and joint infections
− Community acquired pneumonia − Pyelonephritis or prostatitis
(severe) (mild to moderate)
− Complicated intraabdominal − Sepsis in neonates and
infections (mild to moderate) children
− Complicated intraabdominal
infections (severe)
− Hospital acquired pneumonia
− Pyelonephritis or prostatitis
(severe)
CEFTRIAXONE* − Acute bacterial meningitis − Acute invasive bacterial
− Community acquired pneumonia diarrhoea / dysentery
(severe) − Bone and joint infections
− Complicated intraabdominal − Pyelonephritis or prostatitis
infections (mild to moderate) (mild to moderate)
− Complicated intrabdominal − Sepsis in neonates and
infections (severe) children
− Endophthalmitis
− Enteric fever
− Gonorrhoea
− Hospital acquired pneumonia
− Necrotizing fasciitis
− Pyelonephritis or prostatitis
(severe)
CEFUROXIME − Surgical prophylaxis
CIPROFLOXACIN − Acute invasive bacterial diarrhoea / − Cholera
dysentery − Complicated intraabdominal
− Enteric fever infections (mild to moderate)
− Low-risk febrile neutropenia
− Pyelonephritis or prostatitis (mild
to moderate)
CLARITHROMYCIN† Community acquired pneumonia − Pharyngitis
THERAPEUTIC (severe)
ALTERNATIVES: -
ERYTHROMYCIN*
*AS SECOND CHOICE
TREATMENT FOR
PHARYNGITIS IN CHILDREN
(EMLC ONLY)
PIPERACILLIN + − Complicated intraabdominal
TAZOBACTAM infections (severe)
− High-risk febrile neutropenia
− Hospital acquired pneumonia
− Necrotizing fasciitis
VANCOMYCIN − C. difficile infection
Complementary List
Watch group Indications
antibiotics First choice Second choice
CEFTAZIDIME − Endophthalmitis
MEROPENEM* − Acute bacterial meningitis in
THERAPEUTIC neonates
ALTERNATIVES*: - − Complicated intraabdominal
IMIPENEM + CILASTATIN infections (severe)
*COMPLICATED − High-risk febrile neutropenia
INTRAABDOMINAL
INFECTIONS AND HIGH-RISK
FEBRILE NEUTROPENIA
ONLY. MEROPENEM IS THE
PREFERRED CHOICE FOR
ACUTE BACTERIAL
MENINGITIS IN NEONATES.
VANCOMYCIN − Endophthalmitis − Necrotizing − High-risk febrile neutropenia
fasciitis

Reserve group antibiotics


Reserve group antibiotics Indications
First choice Second choice
Ceftazidime + avibactam Carbapenem resistant
Acinetobacter
baumannii
-Carbapenem-resistant
Pseudomonas
aeruginosa
-Carbapenem resistant
Enterobacterales

Colistin -Carbapenem resistant


Acinetobacter
baumannii
-Carbapenem-resistant
Pseudomonas
aeruginosa
-Carbapenem resistant
Enterobacterales

Fosfomycin (intravenous)
Linezolid -Multi-drug resistant
Mycobacterium
tuberculosis
-Vancomycin resistant
Enterococcus
 -Vancomycin resistant
Staphylococcus aureus
-Methicillin resistant
Staphylococcus aureus

Meropenem + vaborbactam Carbapenem resistant


Enterobacterales
-Carbapenem-resistant
Pseudomonas
aeruginosa,
-Carbapenem resistant
Acinetobacter
baumannii
Plazomicin -Carbapenem resistant
Enterobacterales
-Carbapenem-resistant
Pseudomonas
aeruginosa,
-Carbapenem resistant
Acinetobacter
baumannii
Polymyxin B -Carbapenem resistant
Enterobacterales
-Carbapenem-resistant
Pseudomonas
aeruginosa,
-Carbapenem resistant
Acinetobacter
baumannii

ACTIVITY NO 6
INTRODUCTION TO DIFFERENT (EML) AND COMPARISON
BETWEEN WHO AND PAKISTAN’S ESSENTIAL MEDICINE LIST’S.

WHO EML NATIONAL EML DIFFERENCE


A A
abacavir abacavir (ABC)
abacavir + lamivudine abacavir + lamivudine
abiraterone Abiraterone
acetazolamide acetazolamide
acetic acid acetic acid
acetylcysteine Acetylcysteine
acetylsalicylic acid acetylsalicylic acid
acyclovir Acyclovir
adalimumab adalimumab
albendazole Albendazole
alcohol based hand rub alcohol based hand rub
allopurinol allopurinol
all-trans retinoid acid (ATRA) all trans retinoid acid (ATRA)
alteplase alteplase
amidotrizoate amidotrizoate
amikacin amikacin
amiloride amiloride
amiodarone amidarone
amitriptyline amitriptyline
amlodipine amlodipine
amodiaquine amodiaquine
amodiaquine – sulfadoxine + pyrimethamine amodiaquine-sulfadoxine-
amoxicillin pyrimethamine
amoxicillin + clavulanic acid amoxicillin
amphotericin B amoxicillin + clavulanic acid
ampicillin amphotericin B
anastrozole ampicillin
anti-D immunoglobulin anastrozole
anti-rabies immunoglobulin anti-D immunoglobulin
anti-rabies virus monoclonal antibodies Anti rabies immunoglobulin
anti-tetanus immunoglobulin Anti-tetanus immunoglobulin
Anti-venom immunoglobulin Anti-venom immunoglobulin
aprepitant aprepitant
arsenic trioxide arsenic trioxide
artemether artemether
artemether + lumefantrine artemether + lumefantrine
artesunate artesunatre
artesunate + amodiaquine artesunate + amodiaquine
artesunate + mefloquine artesunate + mefloquine
artesunate + pyronaridine tetraphosphate artesunate + pyronaridine
ascorbic acid telraphosphate
asparaginase ascorbic acid
atazanavir + ritonavir asparaginase
atracurium atazanavir
atropine atazanavir + ritonavir
azathioprine atracurium
azithromycin atropine
azathioprine
azithromycin
B B bupropion
barium sulfate barium sulfate
BCG vaccine BCG vaccine
bedaquiline beclometasone
bendamustine bedaquiline
benzathine benzylpenicillin bendamustine
benznidazole benzathine benzylpenicillin
benzoyl peroxide benznidazole
benzyl benzoate benzoyl peroxide
benzylpenicillin benzyl benzoate
betamethasone benzylpenicillin
bevacizumab betamethasone
bicalutamide bevacizumab
biperiden bicalutamide
bisoprolol biperiden
bleomycin bisoprolol
bortezomib bleomycin
budesonide bortezomib
budesonide + formoterol budesonide
bupivacaine budesonide + formoterol
bupropion bupivacaine
C C calcipotriol
caffeine citrate caffeine citrate cefiderocol
calamine calamine
calcipotriol calcium
calcium calcium folinate
calcium folinate calcium gluconate
calcium gluconate capecitabine
capecitabine carbamazepine
carbamazepine carbetocin
carbetocin carboplatin
carboplatin cefalexin
cefalexin cefazolin
cefazolin cefixime
cefiderocol cefotaxime
cefixime ceftazidime
cefotaxime ceftazidime + avibactam
ceftazidime ceftriaxone
ceftazidime + avibactam cefuroxime
ceftriaxone charcoal activated
cefuroxime chlorambucil
charcoal, activated chloramphenicol
chlorambucil chlorhexidine
chloramphenicol chlorine base compound
chlorhexidine chloroquine
chlorine base compound chloroxylenol
chloroquine chlorpromazine
chloroxylenol cholera vaccine
chlorpromazine ciclosporin
cholera vaccine ciprofloxacin
ciclosporin cisplatin
ciprofloxacin clarithromycin
cisplatin clindamycin
clarithromycin clofazimine
clindamycin clomifene
clofazimine clomipramine
clomifene clopidogrel
clomipramine clotrimazole
clopidogrel cloxacillin
clotrimazole clozapine
cloxacillin coagulation factor IX
clozapine coagulation factor WII
coagulation factor IX coal tar
coagulation factor VIII codeine
coal tar colecalciferol
codeine colistin
colecalciferol condoms
colistin copper-containing device
condoms cyclizine
copper-containing device cyclophosphamide
cyclizine cycloserine
cyclophosphamide cytarabine
cycloserine
cytarabine
D D daclatasvir +
dabigatran dabigatran sofosbuvir
dacarbazine dacarbazine
daclatasvir daclatasvir
daclatasvir + sofosbuvir dactinomycin
dactinomycin dapsone
dapsone darunavir
darunavir dasabuvir
dasabuvir dasatinib
dasatinib daunorubicin
daunorubicin deferoxamine
deferoxamine delamanid
delamanid dengue vaccine
dengue vaccine desmopressin
desmopressin dexamethasone
dexamethasone dextran 70
dextran diaphragms
diaphragms diazepam
diazepam diazoxide
diazoxide diethylcabamazine
diethylcarbamazine digoxin
digoxin dihydroartemisinin +piperaquine
dihydroartemisinin + piperaquine phosphate phosphate
diloxanide diloxanide
dimercaprol dimercaprol
diphtheria antitoxin diphtheria antitoxin
diphtheria vaccine diphtheria vaccine
docetaxel docetaxel
docusate sodium docusate sodium
dolutegravir dolutegravir
dolutegravir + lamivudine + tenofovir dolutegravir +
dopamine lamivudine+tenofovir
doxorubicin dopamine
doxycycline doxorubicin
doxycycline
E E empagliflozin
efavirenz efavirenz (EFVoTEFZ) equine rabies-
efavirenz + emtricitabine + tenofovir efavirenz + emtricitabine+tenofovir immunoglobulin
efavirenz + lamivudine + tenofovir efavirenz + lamivudine+tenofovir everolimus
eflornithine eflomithine
empagliflozin emticitabine+tenofovir
emtricitabine + tenofovir enalapril
enalapril enoxaparjn
enoxaparin entecavir
entecavir ephedrine
ephedrine epinephrine (adrenaline)
epinephrine (adrenaline) ergocalciferol
equine rabies immunoglobulin ergometrine
ergocalciferol erotinib
ergometrine erythromycin
erlotinib erythropoiesis-stimulating agents
erythromycin estradiol cypionate
erythropoiesis-stimulating agents +medroxyprogesterone eacetate
estradiol cypionate + medroxyprogesterone ethambutol
acetate ethambutol +isoniazid +
ethambutol pyrazinamide+ rifampicin
ethambutol + isoniazid + pyrazinamide + ethambutol +rsoniazid+ rifampicin
rifampicin ethanol
ethambutol + isoniazid + rifampicin 15 ethrnyleslradrol + levonorgestrel
ethanol ethinylestradiol + norethisterone
ethinylestradiol + etonogestrel ethionamide
ethinylestradiol + levonorgestrel ethosuximide
ethinylestradiol + norethisterone etonogestrel-releasing implant 47
ethionamide etoposide
ethosuximide
etonogestrel-releasing implant
etoposide
everolimus
F F Fluoride
fentanyl fentanyl
ferrous salt ferrous salt
ferrous salt + folic acid ferrous salt + folic acid
fexinidazole fexinidazole
filgrastim filgrastim
fluconazole fluconazole
flucytosine flucytosine
fludarabine fludarabine
fludrocortisone fludrocortisone
fluorescein fluorescein
fluoride fluorouracil
fluorouracil fluoxetine
fluoxetine fluphenazine
fluphenazine folic acid
folic acid fomepizole
fomepizole fosfomycin
fosfomycin fresh-frozen plasma
fresh-frozen plasma furosemide
furosemide
G G glass ionomer
gemcitabine gemcitabine cement
gentamicin gentamicin
glass ionomer cement glecaprevir + pibrentasvir
glecaprevir + pibrentasvir gliclazide
gliclazide glucagon
glucagon glucose
glucose glucose with sodium chloride
glucose with sodium chloride glutaral
glutaral glyceryl trinitrate
glyceryl trinitrate griseofulvin
griseofulvin
H H -
Haemophilus influenzae type b vaccine Haemophilus influenzae type b
haloperidol vaccine
halothane haloperidol
heparin sodium halothane
hepatitis A vaccine heparin sodium
hepatitis B vaccine hepatitis A vaccine
human papilloma virus (HPV) vaccine hepatitis B vaccine
hydralazine human papilloma virus (HPV)
hydrochlorothiazide vaccine
hydrocortisone hydralazine
hydroxy cobalamin hydrochlorothiazide
hydroxyy carbamide hydrocortisone
hydroxyl chloroquine hydroxy cobalamin
hyoscine butyl bromide hydroxyy carbamide
hyoscine hydro bromide hydroxyl chloroquine
hyoscine butyl bromide
hyoscine hydro bromide
I I ibrutinib
ibrutinib ibuprofen isoniazid +
ibuprofen ifosfamide rifapentine
ifosfamide imatinib
imatinib influenza vaccine
influenza vaccine insulin injection (soluble)
insulin injection (soluble) intermediate-acting insulin
intermediate-acting insulin intraperitoneal dialysis solution (of
intraperitoneal dialysis solution (of appropriat appropriat
composition) composition)
iodine iodine
iohexol iohexol
ipratropium bromide ipratropium bromide
innotecan innotecan
isoflurane isoflurane
isoniazid isoniazid
isoniazid + pyrazinamide + rifampicin isoniazid + pyrazinamide +
isoniazid + pyridoxine + sulfamethoxazole + rifampicin
trimethoprim isoniazid + pyridoxine +
isoniazid + rifampicin sulfamethoxazole + trimethoprim
isoniazid + rifapentine isoniazid + rifampicin
isosorbide dinitrate isosorbide dinitrate
itraconazole itraconazole
ivermectin ivermectin
J J
Japanese encephalitis vaccine Japanese encephalitis vaccine
K K
Ketamine ketamine
L L long-acting insulin
lactulose lactulose analogues
lamivudine lamivudine
lamivudine + zidovudine lamivudine + zidovudine
lamotrigine lamotrigine
latanoprost latanoprost
ledipasvir + sofosbuvir ledipasvir + sofosbuvir
lenalidomide lenalidomide
leuprorelin leuprorelin
levamisole levamisole
levodopa + carbidopa levodopa + carbidopa
levofloxacin levofloxacin
levonorgestrel levonorgestrel
levonorgestrel-releasing implant levonorgestrel-releasing implant
levonorgestrel-releasing intrauterine system levonorgestrel-releasing
levothyroxine intrauterine system
lidocaine levothyroxine
lidocaine + epinephrine (adrenaline) lidocaine
linezolid lidocaine + epinephrine
lisinopril + amlodipine (adrenaline)
lisinopril + hydrochlorothiazide linezolid
lithium carbonate lisinopril + amlodipine
long-acting insulin analogues lisinopril + hydrochlorothiazide
loperamide lithi loperamide
lopinavir + ritonavir lopinavir + ritonavir
loratadine loratadine
lorazepam lorazepam
losartan losartan
Lugol's solution Lugol's solution um carbonate
M M meglumine
magnesium sulfate magnesium sulfate antimoniate
mannitol mannitol micafungin
measles vaccine measles vaccine multiple
mebendazole mebendazole micronutrient
medroxyprogesterone acetate medroxyprogesterone acetate supplement
mefloquine mefloquine
meglumine antimoniate meglumine iotroxate
meglumine iotroxate melarsoprol
melarsoprol melphalan
melphalan meningococcal meningitis vaccine
meningococcal meningitis vaccine mercaptopurine
mercaptopurine meropenem
meropenem meropenem + vaborbactam
meropenem + vaborbactam mesna
mesna metformin
metformin methadone
methadone methimazole
methimazole methotrexate
methotrexate methyldopa
methyldopa methylprednisolone
methylprednisolone methylthioninium chloride
methylthioninium chloride (methylene blue) (methylene blue)
metoclopramide metoclopramide
metronidazole metronidazole
micafungin miconazole
miconazole midazolam
midazolam mifepristone – misoprostol
mifepristone – misoprostol miltefosine
miltefosine misoprostol
misoprostol morphine
morphine moxifloxacin
moxifloxacin multiple micronutrient powder
multiple micronutrient powder mumps vaccine
multiple micronutrient supplement mupirocin
mumps vaccine
mupirocin
N N
Naloxone Naloxone
natamycin natamycin
neostigmine neostigmine
nevirapine nevirapine
niclosamide niclosamide
nicotinamide nicotinamide
nicotine replacement therapy (NRT) nicotine replacement therapy
nifedipine (NRT)
nifurtimox nifedipine
nilotinib nifurtimox
nitrofurantoin nilotinib
nitrous oxide nitrofurantoin
nivolumab nitrous oxide
norethisterone enantate nivolumab
normal immunoglobulin norethisterone enantate
nystatin normal immunoglobulin
nystatin
O O -
ofloxacin ofloxacin
ombitasvir + paritaprevir + ritonavir ombitasvir + paritaprevir +
omeprazole ritonavir
ondansetron omeprazole
oral rehydration salts ondansetron
oral rehydration salts – zinc sulfate oral rehydration salts
oseltamivir oral rehydration salts – zinc sulfate
oxaliplatin oseltamivir
oxamniquine oxaliplatin
oxygen oxamniquine
oxytocin oxygen
oxytocin
P P paliperidone
paclitaxel paclitaxel
paliperidone p-aminosalicylic acid
p-aminosalicylic acid pancreatic enzymes
pancreatic enzymes paracetamol
paracetamol paromomycin
paromomycin pegaspargase
pegaspargase pegylated interferon alfa 2a
pegylated interferon alfa 2a penicillamine
penicillamine pentamidine
pentamidine permethrin
permethrin pertussis vaccine
pertussis vaccine phenobarbital
phenobarbital phenoxymethylpenicillin
phenoxymethylpenicillin phenytoin
phenytoin phytomenadione
phytomenadione pilocarpine
pilocarpine piperacillin + tazobactam
piperacillin + tazobactam platelets
platelets plazomicin
plazomicin pneumococcal vaccine
pneumococcal vaccine podophyllum resin
podophyllum resin poliomyelitis vaccine
poliomyelitis vaccine polymyxin B
polymyxin B potassium chloride
potassium chloride potassium ferric hexacyano-
potassium ferric hexacyano-ferrate(II) -2H20 ferrate(II) -2H20 (Prussian blue)
(Prussian blue) potassium iodide
potassium iodide potassium permanganate
potassium permanganate povidone iodine
povidone iodine praziquantel
praziquantel prednisolone
prednisolone primaquine
primaquine procaine benzylpenicillin
procaine benzylpenicillin procarbazine
procarbazine progesterone vaginal ring
progesterone vaginal ring proguanil
proguanil propofol
propofol propranolol
propranolol propylthiouracil
propylthiouracil prostaglandin E1
prostaglandin E1 protamine sulfate
protamine sulfate pyrantel
pyrantel pyrazinamide
pyrazinamide pyridostigmine
pyridostigmine pyridoxine
pyridoxine pyrimethamine
pyrimethamine
Q Q
Quinine Quinine
R R rasburicase
rabies vaccine rabies vaccine
raltegravir raltegravir
ranitidine ranitidine
rasburicase realgar-Indigo naturalis formulation
realgar-Indigo naturalis formulation red blood cells
red blood cells retinol
retinol ribavirin
ribavirin riboflavin
riboflavin rifabutin
rifabutin rifampicin
rifampicin rifapentine
rifapentine risperidone
risperidone ritonavir
ritonavir rituximab
rituximab rotavirus vaccine
rotavirus vaccine rubella vaccine
rubella vaccine
S S silver diamine
salbutamol salbutamol fluoride
salicylic acid salicylic acid sumatriptan
selenium sulfide selenium sulfide
senna senna
silver diamine fluoride silver sulfadiazine
silver sulfadiazine simvastatin
simvastatin sodium calcium edetate
sodium calcium edetate sodium chloride
sodium chloride sodium fluoride
sodium hydrogen carbonate sodium hydrogen carbonate
sodium lactate sodium lactate
sodium nitrite sodium nitrite
sodium nitroprusside sodium nitroprusside
sodium stibogluconate sodium stibogluconate
sodium thiosulfate sodium thiosulfate
sofosbuvir sofosbuvir
sofosbuvir + velpatasvir sofosbuvir + velpatasvir
spectinomycin spectinomycin
spironolactone spironolactone
streptokinase streptokinase
streptomycin streptomycin
succimer succimer
sulfadiazine sulfadiazine
sulfadoxine + pyrimethamine sulfadoxine + pyrimethamine
sulfamethoxazole + trimethoprim sulfamethoxazole + trimethoprim
sulfasalazine sulfasalazine
sumatriptan suramin sodium
suramin sodium surfactant
surfactant suxamethonium
suxamethonium
T T Tacrolimus
tacrolimus tamoxifen Trimethoprim
tamoxifen telmisartan + amlodipine
telmisartan + amlodipine telmisartan + hydrochlorothiazide
telmisartan + hydrochlorothiazide tenofovir disoproxil fumarate
tenofovir disoproxil fumarate terbinafine
terbinafine testosterone
testosterone tetanus vaccine
tetanus vaccine tetracaine
tetracaine tetracycline
tetracycline thalidomide
thalidomide thiamine
thiamine tick-borne encephalitis vaccine
tick-borne encephalitis vaccine timolol
timolol tioguanine
tioguanine tiotropium
tiotropium tranexamic acid
tranexamic acid trastuzumab
trastuzumab triclabendazole
triclabendazole tropicamide
trimethoprim tuberculin, purified protein
tropicamide derivative (PPD)
tuberculin, purified protein derivative (PPD) typhoid vaccine
typhoid vaccine
U U
ulipristal ulipristal
urea urea
V V varenicline
valganciclovir valganciclovir
valproic acid (sodium valproate) valproic acid (sodium valproate)
vancomycin vancomycin
varenicline varicella vaccine
varicella vaccine vecuronium
vecuronium verapamil
verapamil vinblastine
vinblastine vincristine
vincristine vinorelbine
vinorelbine voriconazole
voriconazole
W W
warfarin warfarin
water for injection water for injection
whole blood whole blood
X X
Xylometazoline Xylometazoline
Y Y
Yellow fever vaccine Yellow fever vaccine
Z Z
zidovudine zidovudine
zinc sulfate zinc sulfate
zoledronic acid zoledronic acid

ACTIVITY NO 7
THE PROCEDURE FOR CONDUCTION ABC/VEN ANALYSIS WITH
PRACTICE EXAMPLE.
Conduct analysis of the following given example of drugs used in hospital.

Drug Name Price Quantity Total


Strength Dosage Per Dispensed Cost
Package
Package Size Form US$ in 1995 US$
Ranitidine Hydrochloride 150 mg N100 Tab $8.00 500 $4,000.00
Bendazol 0.5% 2 ml N10 Inj $0.50 5000 $2,500.00
Cocarboxylase 50 mg 3 ml N3 Inj $1.25 1000 $1,250.00
Metoclopramide Hydrochloride 10 mg N40 Tab $1.67 1200 $2,004.00
Solcoseril 2 ml N25 Inj $20.12 700 $14,084.00
Verapamil Hydrochloride 80 mg N100 Tab $5.00 1200 $6,000.00
Nandrolone Decanoate 50 mg 1 ml Inj $1.74 800 $1,392.00
Metamizole 50% 1 ml N10 Inj $0.30 2000 $600.00
Nitrofurantoin 100 mg N10 Tab $0.15 3000 $450.00
Inosine 200 mg N100 Tab $20.00 800 $16,000.00
Insulin HM 10 ml 40 IU/ml Inj $5.50 2000 $11,000.00
Cefotaxime Sodium 1 g Inj $2.40 2000 $4,800.00
Prednisolone 30 mg N3 Inj $1.21 1900 $2,299.00
Digoxin 0.25 mg N50 Tab $1.00 600 $600.00
Drotaverine Hydrochloride 0.04 N100 Tab $2.15 5000 $10,750.00
Nystatin 500,000 U N25 Tab $0.73 3000 $2,190.00
Ampicillin 250 mg N24 Tab $1.25 1500 $1,875.00
Allylestrenol 5 mg N20 Tab $1.63 300 $489.00
Inosine 2% 5 ml N10 Inj $1.57 3000 $4,710.00
Chlordiazepoxide 10 mg N50 Tab $0.56 800 $448.00
Isradipine 5 mg N30 Caps $16.21 600 $9,726.00
TOTAL $97,167.00

To conduct ABC & VEN analysis the following procedure is followed for any given drugs in a
hospital.
1. Prepare a list of all drugs used in the hospital.

For each drug list the name, strength, package size, dosage form, package price, quantity
dispensed (annual consumption) and total cost. Determine the total cost for each drug by
multiplying the quantity dispensed (number of packages consumed annually) times the price per
package.

2. Categorize each drug as vital, essential, or non-essential.

This step is the VEN analysis and is conducted for the purpose of increasing effectiveness of
drug utilization, and for determining which drugs to include in the hospital formulary or drug list.
The classification is based on a drug’s importance in treating the patient, for example:

 Vital drugs: Drugs that are lifesaving (e.g., vaccines), and those necessary for life support
(e.g. Insulins, digoxin, some antibiotics, cytotoxic, anti-shock, etc.).
 Essential drugs: Drugs that are effective for treatment of less life threatening, but still
severe, diseases (e.g., antibiotics, ranitidine, chloroquine, phenytoin, etc.).
 Non-essential drugs: Drugs used for treatment of mild diseases, drugs with questionable
effectiveness, and high cost drugs used for symptomatic therapy.
3. Rearrange drugs according to decreasing total cost to the hospital.

Using total cost as the basis, list drugs according to their decreasing cost to the hospital. This will
place the most costly drugs at the top of the list. If using a computer spreadsheet, the sort
function will rapidly perform this task.

4. Calculate the percentage of total hospital drug budget spent for each drug.

This step involves two calculations for each drug:

(1) Total Cost % is determined by dividing the amount in the total cost column for each
drug by the total cost for all 21 drugs.

(2) Cumulative % is a sum calculated by adding the total cost % of a drug to the cumulative
% of the previous drug as you descend the drug list.

VEN Drug Name Dosage Price Quantity Total Total Cumulative


Category Strength Form Per Dispensed Cost Cost %
(VEN) Package Size Package in 1995 US$ %
US$
N Inosine 200 mg N100 tab $20.00 800 $16,000.00 16.5% 16.5%
N Solcoseril 2 ml N25 inj $20.12 700 $14,084.00 14.5% 31.0%
V Insulin HM 10 ml 40 IU/ml inj $5.50 2000 $11,000.00 11.3% 42.3%
N Drotaverine Hydrochloride tab $2.15 5000 $10,750.00 11.1% 53.4%
0.04 N100
E Isradipine 5 mg N30 caps $16.21 600 $9,726.00 10.0% 63.4%
V Verapamil Hydrochloride tab $5.00 1200 $6,000.00 6.2% 69.6%
80 mg N100
V Cefotaxime Sodium 1 g inj $2.40 2000 $4,800.00 4.9% 74.5%
N Inosine 2% 5 ml N10 inj $1.57 3000 $4,710.00 4.8% 79.4%
E Ranitidine Hydrochloride tab $8.00 500 $4,000.00 4.1% 83.5%
150 mg N100
N Bendazol 0.5% 2 ml N10 inj $0.50 5000 $2,500.00 2.6% 86.0%
V Prednisolone 30 mg N3 inj $1.21 1900 $2,299.00 2.4% 88.4%
E Nystatin 500,000 U N25 tab $0.73 3000 $2,190.00 2.3% 90.7%
E Metoclopramide tab $1.67 1200 $2,004.00 2.1% 92.7%
Hydrochloride 10 mg N40
V Ampicillin 250 mg N24 tab $1.25 1500 $1,875.00 1.9% 94.7%
E Nandrolone Decanoate 50 inj $1.74 800 $1,392.00 1.4% 96.1%
mg 1 ml
N Cocarboxylase 50 mg 3 ml inj $1.25 1000 $1,250.00 1.3% 97.4%
N3
E Metamizole 50% 1 ml N10 inj $0.30 2000 $600.00 0.6% 98.0%
V Digoxin 0.25 mg N50 tab $1.00 600 $600.00 0.6% 98.6%
E Allylestrenol 5 mg N20 tab $1.63 300 $489.00 0.5% 99.1%
E Nitrofurantoin 100 mg N10 tab $0.15 3000 $450.00 0.5% 99.6%
E Chlordiazepoxide 10 mg tab $0.56 800 $448.00 0.5% 100.0%
N50
TOTAL $97,167.00 100.0%

5. Review the ABC/VEN-analyses results:

The hospital X spent $97,167 for purchases of drugs. When placing the drugs according to the
VEN system, six of the 21 drugs were included in the category of (V)ital drugs (insulin,
verapamil, cefotaxime, prednisolone, ampicillin, digoxin). Nine drugs were included in the
category of (E)ssential drugs (isradipine, ranitidine, nystatin, metoclopramide, nandrolone,
metamizole, allylestrenol, nitrofurantoin, chlordiazepoxide). The group of (N)on-essential drugs
was represented by six drugs (bendazol, drotaverine, inosine, solcoseril, cocarboxylase).

The ABC analysis was conducted with the purpose of reducing expenditures and increasing
effectiveness of drug utilization. This analysis showed that the largest portion of money, 79%,
was spent for purchases of eight drugs (Class A-up to 80% of total costs). When analyzing the
drugs from this class, it was found that it included both vital drugs (insulin, verapamil, and
cefotaxime --22.2% of total budget spent), as well as non-essential drugs, (inosine, solcoseril,
and drotaverine, representing 46.9% of budget). For the drugs from Classes B and C, 20.6% of
the budget was spent. These classes also included vital drugs (prednisolone, ampicillin, and
digoxin), essential drugs (nystatin, ranitidine, etc.), as well as non-essential drugs (bendazol and
cocarboxylase).

The analysis shows the structure of drug expenditures in the hospital, and allows for introduction
of reforms in drug purchasing policy, and for shifting budget funds for the purchase of vital
drugs. By limiting the use of such ineffective drugs as solcoseril, inosine, and drotaverine,
expenditures can be significantly reduced.

This example of ABC-analysis demonstrates that such an analysis may become an effective tool
for selecting drug classes for the initial formulary list review, and for corrections in purchasing
policy.

ACTIVITY NO:8
Designing a DUR evaluation and establish DUR criteria of
different drugs.
EXAMPLE OF ESTABLISHED DUR CRITERIA ON DATA COLLECTION FORM FOR
AMIKACIN
DATE: DRUG: Data collector’s initials:
Patient Chart No

Diagnosis
Age/Sex/Weight

Date Treated

CRITERIA AND INDICATORS Threshold Observed

Justification for Drug Being Prescribed:


1. Serious infections caused by susceptible strains of 100% YES NO YES NO YES NO YES NO
aerobic gram-negative bacteria resistant to gentamicin
and tobramycin
2. Suspected serious gram-negative infections acquired 100%
in the hospital with high resistance rates to gentamicin
and tobramycin
3. In combination with an anti-pseudomonad penicillin
100%
when treating serious pseudomond infections

Process Indicators:
4. Obtain serum creatinine prior to therapy or within 24 100% YES NO YES NO YES NO YES NO
hours of initiation of therapy 5. Loading dose of 7.5
mg/kg (IV or IM) based on ideal body weight
6. Maintenance dosage range of 15 mg/kg/day ideal 100%
weight (exception:renal compromise)
7. Therapy changed to tobramycin, gentamicin, or other 100%
drug if culture and sensitivity indicates less expensive or
more appropriate drug
Outcome Indicators:
8. Clinical improvement noted in patient medical 100% YES NO YES NO YES NO YES NO
records
100%
9. Fever reduction to normal within 72 hours

EXAMPLE OF ESTABLISHED DUR CRITERIA ON DATA COLLECTION


FORM FOR IV AMINOPHYLLINE
DATE: DRUG: Data collector’s initials:
Patient Chart No

Diagnosis

Age/Sex/Weight

Date Treated
CRITERIA AND INDICATORS Threshold Observed

Justification for Drug Being Prescribed:


1. Shortness of breath, wheezing and dyspnea, 100% YES NO YES NO YES NO YES NO

acute status asthmaticus, or other evidence of


bronchospasm after a failure to respond to
epinephrine
2. Poor response to oral bronchodilators or
100%
inability of patient to take oral 100%
bronchodilator
Process Indicators:
YES NO YES NO YES NO YES NO
4. Theophylline serum level obtained prior to 100%
initiation of therapy in patients on oral
theophylline drugs 100%
5. Loading dose (use lean body weight): 6.25
mg/kg (IV) or 3 mg/kg IV if received theophylline 100%
in previous 24 hours
6. Initial maintenance dosage (use lean body 100%
weight): (a) children 1-9 years: 1.0 mg/kg/hr (b)
children >9 years (and adult smokers): 0.75
mg/kg/hr (c) adolescents and adults (non
smokers): 0.5 mg/kg/hr (d) adults with congestive
heart failure or liver dysfunction: 0.25 mg/kg/hr
7. Serum levels obtained and adjusted to maintain 100%
levels of 10 to 20 mcg/ml (1st level obtained after
24 hours of therapy)
8. Therapy changed to oral theophylline within 48 100%
hours if patient able to 100% take oral therapy
(theophylline dose = 80% of aminophylline dose;
this is a cost containment measure)
Outcome Indicators:
YES NO YES NO YES NO YES NO
9. Clinical improvement noted in patient medical 100%
records

EXAMPLE OF ESTABLISHED DUR CRITERIA ON DATA COLLECTION


FORM FOR DIGOXIN
DATE: DRUG: Data collector’s initia’S
Patient Chart No

Diagnosis

Age/Sex/Weight
Date Treated

CRITERIA AND INDICATORS Threshold Observed

Justification for Drug Being Prescribed: YES NO YES NO YES NO YES NO


1. Congestive heart failure 100%
2. Atrial tachyarrhythmias
100%
Process Indicators:
3. Determine following tests prior to therapy: serum 100% YES NO YES NO YES NO YES NO
creatinine, electrolytes, and electrocardiogram (low
potassium levels may decrease threshold for toxicity)
4. Maintenance dose: 0.125 to 0.5 mg daily 100%
5. Serum levels are drawn at least eight hours after an
oral dose (preferably in the AM prior to scheduled dose 100%
for patients on maintenance therapy)
6. Serum levels are drawn if disease worsens or: (a) 100%
suspected non-compliance, confirmation of overdose or
suspected toxicity (b) unstable renal function or change
in renal function during therapy (c) possible interaction
with other drug (e.g., quinidine, amiloride, calcium
channel blocker, amiodarone, amrinone, thiazides,
thyroid hormones)
7. Therapy is evaluated/adjusted for: anorexia, nausea, 100%
visual disturbances, agitation, nervousness, psychoses,
and disrhythmias (ventricular, atrial and brady
arrhythmias)
100%

Outcome Indicators:
8. Clinical improvement noted in patient medical 100% YES NO YES NO YES NO YES NO
records

EXAMPLE OF ESTABLISHED DUR CRITERIA ON DATA COLLECTION


FORM FOR METAPROTERENOL
DATE: DRUG: Data collector’s initials:
Patient Chart No

Diagnosis

Age/Sex/Weight
Date Treated

CRITERIA AND INDICATORS Threshold Observed

Justification for Drug Being Prescribed:


1. Symptomatic treatment of asthma and acute 100% YES NO YES NO YES NO YES NO
bronchospasm
2. Symptomatic management of chronic bronchospastic
pulmonary diseases

100%

Process Indicators:
3. Use no longer than 24 hours in acute setting (IPPB, 100% YES NO YES NO YES NO YES NO
nebulized)
4. Nebulized inhalation solutions changed to inhalation
aerosol when patient able to use self-therapy 100%
6. Patient instructed on appropriate use of inhaler when
on aerosol 100%
7. Dosage reduced if side effects are bothersome or
clinically evident: e.g., tachycardia, tremor, headache, 100%
nervousness, palpitation, hypertension, dizziness, nausea
and vomiting
8. Caution is noted when administered concomitantly
with beta agonists,
sympathomimetics or with beta-blockers (may
antagonize activity)
9. Dosage is adjusted or therapy discontinued in 100%
response to: adverse effects, drug interactions, poor
response to therapy, or poor compliance to therapy

100%

Outcome Indicators:
10. Breathing improvement noted in patient medical 100% YES NO YES NO YES NO YES NO
records
11. Clinical improvement in pulmonary function (FEVI)

EXAMPLE OF ESTABLISHED DUR CRITERIA ON DATA COLLECTION FORM


FOR USE OF ANTIBIOTIC IN SURGICAL PROPHYLAXIS
DATE: DRUG: Data collector’s initials:
Patient Chart No

Diagnosis

Age/Sex/Weight
Date Treated

CRITERIA AND INDICATORS Threshold Observed

Justification for Drug Being Prescribed:


1. Class of surgery: clean contaminated, dirty 100% YES NO YES NO YES NO YES NO

contaminated, ruptured, or gangrenous


2. Antibiotic on approved list for surgical
prophylaxis
100%

Process Indicators:
YES NO YES NO YES NO YES NO
3. Dose given only one time, and not more than 100%
45 min. before incision
4. Antibiotic administered if surgery is prolonged, 100%
4 or more hours later
5. Post operative doses specified for no more than 100%
24 hours
6. Antibiotic change recommended due to: 100% 100%
(a) adverse reaction (b) decreased renal function
(c) drug interaction (d) cost effectiveness
increased (e) documented infection
7. Nosocomial infection is documented prior to
non-surgical prophylaxis use of antibiotic
100%

100%

Outcome Indicators: None

ACTIVITY NO: 9
TO SOLVE NUMERICAL PROBLEMS RELATED TO THE DRUG
DIGOXIN.
PROBLEM NO 1:
A 72 year old patient having 83 kg weight, 5ft 11inch in height, is admitted to the hospital for the
treatment of community acquired pneumonia. While in his stay at hospital he develops atrial
fibrillation, and the decision is made to treat him with digoxin to provide ventricular rate control.
His serum creatinine concentration is 2.5mg/dL and is stable. Calculate the intravenous loading
dose and oral maintenance dose that will achieve a C ss of 1.5ng/mL. The patient is within 30% of
his ideal body weight.
SOLUTION:-
 Age = 72y
 Weight 83kg
 Height 5ft 11inches
 Serum creatinine = 2.5mg/dL
 Loading Dose =?
 Maintenance dose =?

 Ideal body weight (IBW) = 55 + 2.3 (Height-60)


= 55+ 2.3 (71-60)
=80.3Kg

( 140− Age ( y ) ) ×Weight (kg)


 Creatinine Clearance (Clcr) =
S cr ×72

( 140−72 ) ×83
=
2.5 × 72

=31ml/min.

 Therefore Clearance is given by CL = 1.303 (Clcr. ml/min) + Clin


= 1.303 ( 31) + 40
= 80ml/min

 Volume of distribution is calculated as (Vd) = 226 + ¿]

298(31)
= 226 +
29.1+ 31

= 380L
D
 Maintenance Dose = =C ss Cl / F where F = 0.7
τ

= [(1.5mcg/L)(80mL/min)(60min/h)(24 h/day)] / [0.7(1000ml/L)]


= 247mcg/day rounded to 250mcg/day
 Loading Dose (LD) = Css× Vd

= 1.5 × 380

= 570mcg rounded to 500mcg

PROBLEM NO 2:
This patient responded to digoxin therapy, and he was discharged after resolution of his
pneumonia. A month later he was followed up in the clinic with moderate nausea, possibly a
result of digoxin toxicity. His heart rate was 51 beats per minute. A steady state digoxin
concentration was determined and reported as 2.2mcg/L. calculate the new modified dose for this
patient to achieve a Css of 1.5mcg/L.
SOLUTION:-
 New serum concentration Css(new) = 1.5mcg/L
 Old serum concentration Css(old) = 2.2mcg/L
 Old digoxin dose = 250mcg/d
 New dose =?

 New dose (Dnew) = Dold (Css.new) / (Css.old)

= 250 (1.5) / (2.2)

= 170 mcg/day.

ACTIVITY NO 10
TO SOLVE NUMERICAL PROBLEM RELATED TO THE DRUG THEOPHYLLINE.

PROBLEM NO 1:
A 55 year old, 70kg man with liver cirrhosis was prescribed a loading dose of theophylline
350mg intravenously over 20-30 minutes, followed by a maintenance dose of 15 mg/h of
theophylline as a continuous infusion. The infusion began at 9am, blood samples were obtained
at 10 am and 4pm, and the clinical laboratory reported the theophylline serum concentrations as
10.9 and 12.3 mg/L respectively. The patient’s Vd is estimated at 0.5L/kg.
SOLUTION:-
 Loading dose =350mg
 Maintenance dose = 15mg/h
 1st blood sample withdrawn (t1) = 10am or at10h
 2nd blood sample withdrawn(t2) = 4pm or at16h
 Serum concentration(c1) = 10.9mg/L
 Serum concentration(c2) = 12.3mg/L
 Volume of distribution(Vd) = 0.5L/kg

 Formula used to calculate clearance using theophylline concentrations is given by:

2 ko 2Vd (C 1+C 2 )
 CL = +
C1 +C 2 ( C1 +C 2 ) (t 2 −t 1 )

Putting the values in the formula:-

2(15) 2 ( 0.5× 70 ) (10.9−12.3)


 CL = +
10.9+12.3 ( 10.9+12.3 )(16−10)

=1.2931 -0.7040
=0.589L/h

 ko = CssCL

= 15×0.59

=9mg/h theophylline
If theophylline is to be given as aminophylline salt form, the dose would need to be changed to
reflect the fact that aminophylline contains only 85% theophylline.
 ko = 9mg/h theophylline/0.85 = 11mg/h aminophylline.

PROBLEM NO 2:
Calculate the new theophylline dose for a patient receiving 200mg of sustained-release oral
theophylline every 12hours with a theophylline steady state serum concentration of 9.5mcg/mL.
What dose is required to achieve a new steady state serum concentration equal to 15mcg/mL?
SOLUTION:
 Old dose = 200mg
 Old steady state concentration (Css(old)) = 9.5mcg/mL
 New steady state concentration (Css(new)) = 12mcg/mL
 New dose =?

The following formula is used in this case i.e.

 Dnew = Dold (Css(new) / Css(old))

=200 (15) / 9.5

=316mg rounded to 300mg


The new theophylline dose would be 300mg every 12 hours.

ACTIVITY NO 11
TO SOLVE NUMERICAL PROBLEMS RELATED TO THE DRUG GENTAMYCIN
AND VANCOMYCIN.

PROBLEM NO 1:
A 65 year old patient having 90kg weight is diagnosed with gram –ve pneumonia. His height is
6ft, his serum creatinine concentration is 2.1mg/dl. Conclude a conventional gentamycin dosing
regimen for the patient to provide peak and trough concentration of 8mg/dl and 1.5mg/dl
respectively.
SOLUTION:-
 Age=65Y
 Weight=90kg
 Height=6ft or 6×12= 72inches
 Serum creatinine=2.1mg/dL
 Cpmaxss=8mg/L
 Cpminss=1.5mg/L

(140−Age) × wt (kg)
 Clearance creatinine (Clcr) = 72 × ( C s ) cr ( mg ) ¿
dL
¿
( 140−65 ) × 90
=
72× 2.1
= 44.642 ml/min
 Ideal Body Weight= 50+ 2.3 [Height (inches)-60]
= 50+2.3 (72-60)
= 77.6kg.
 K= 0.00293 (Clcr) + 0.014
=0.00293 (44.64) + 0.014
= 0.14h
 T1/2 =0.693K
=0.693 × 0.14
= 4.78h
 Vd = 0.26L/kg
=0.26×90
=23.4L
 τ = [ lnCpmax(ss) - lnCpmin(ss) / K ] + T
= [ln (8) – ln (1.5)] / 0.14 + 1
= 12.95h 12h
− Kτ
1−e
 Dose (D) = T×K×Vd×Cpmax(ss) − KT
1−e
−(0.14 )×12
1−e
= 1 × 0.14× 8 × 23.4 ( )
1−e− 0.14 × 1
0.8136
= 26.208 × 0.104

= 163.22 mg 170 mg.


 Loading Dose = Vd × Cpmax(ss)
= 187.2mg

PROBLEM NO 2:-
A Patient was prescribed with 140mg gentamycin every 12 for the treatment of gram –ve
pneumonia. At steady state peak and trough concentration was obtained before and after the 4 th
dose i.e. equal to 2.8mg/L and 8.5mg/L. the S cr value was 2.5mg/dl. Patient was clinically
improving does he require any modification in his dose? If yes, then what is the new dosage
regimen?

SOLUTION:
 Dose of gentamycin = 140mg
 Dose interval (τ ) = 12h
 Cpmax(ss) =8.5mg/L
 Cpmin(ss) = 2.8mg/L
 Scr = 2.5mg/dl
ln Cmax (ss )−ln Cmin ⁡( ss)
 K=
τ−T

ln ( 8.5 )−ln(2.8)
=
12−1

= 0.1009/h
D
 Vd = T ( )
(1−e−Kτ )

K ¿¿

= ( 1401 )(1−e
−0.10019 ×12
)
−0.10019×1
0.10019(8.5−2.8 e )

= 22.34L

 DOSE MODIFICATION:
 τ =¿[lnCpmax(ss) – lnCpmin(ss) / K] + 1
= [ln (8.5) – ln (1.5) / 0.10019] + 1
= 11.0834 + 1
= 17.708h

1−e− Kτ
 DOSE = T.K.Vd. Cpmax(ss) .
1−e− KT

1−e−0.1009 ×17.57
= 1 × 0.1009 × 22.34 × 8 [ −0.1009×1 ]
1−e

= 18.032 × 8.6494

= 156.15mg

160mg

PROBLEM NO 3:-
Ms. HJ is a 65 Year old, 68kg, 5ft 4inch tall patient who has developed a surgical wound
infection with S. aureus the suspected pathogen. Her serum creatinine concentration is 1.8 mg/dL
and stable. Compute a vancomycin dosage regimen that would provide approximate peak
(obtained 1 hour after a 1 hour infusion) and trough concentrations of 30 and 7mg/L,
respectively. The patient is within 30% of her ideal body weight.
SOLUTION:-
 Age = 65Y
 Weight 68kg
 Height = 5ft 4 inches, 64inches
 Scr = 1.8mg/dL
 Cpss.max = 30mg/L
 Cpss.max = 7mg/L
 Ideal body weight (IBW) = 45 + 2.3 (Height-60)
= 45 + 2.3 (64inches-60)
= 54kg

 Creatinine Clearance (CLcr) = 0.85 ¿ ¿

0.85 (140−65 ) ×68


=
72 ×1.8
= 33ml/min.

 CLcr =0.695 (CLcr in ml/min/kg) + 0.05


= 0.695 (33/ml/mim/kg) + 0.05
=0.387mL/min/kg.

 K= Cl/Vd
=[(o.387ml/min/kg)(68kg)(60min/h)] /[(48L)(1,000mL/L)]
= 0.033h-1
 τ =¿[lnCpmax(ss) – lnCpmin(ss) / K]
=(ln 30mg/L – ln 7mg/L) / 0.033
= 44h rounded to 48h

 D = cpss.max Vd (1 – e-kƮ )
=(30)(48)(1-e-(0.033)(48) )
=1145mg rounded to 1,200mg.

 LD = Vd. Cpmax.ss
= 1440mg rouded to 1450mg

Therefore, the prescribed dose of Vancomycin would be 1200mg every 48 h administered as a 1-


hour infusion.
PROBLEM NO 4:
Ms. H was prescribed vancomycin 1200mg every 48 h (Infused over 1 hour) for the treatment of
surgical wound infection. Steady state trough and peak values( peak value obtained 1h after the
infusion) were obtained before and after the third dose was given ( more than 3-5 estimated half-
lives), respectively, an equaled Cmin.ss = 2.5mg/L and Cmax.ss = 22.4md/L. clinically the
patient has improved but the patient wa still febrile. Because of this, a modified dosage regimen
with a Cmax.ss = 30mg/L and Cmin.ss = 7mg/L was suggested to maintain trough
concentrations 3-5 times above the MIC for the suspected pathogen.
SOLUTION:
 Dose = 1200mg
 Dose interval = 48h
 Cmin.ss = 2.5mg/dL
 Cmin.ss = 22.4mg/dL

 K =(lnCmax.ss –ln Cmin.ss) / τ −Tmax


= (ln 22.4 – ln 2.5) (48-2)
= 0.048h

 T1/2 =0.693/k
=0.693/0.048
= 14.4h

D
 VD = Cmax−Cmin

=1200/(22.4-2.5)
= 60L
 To achieve a desired serum concentration the patient;s actual kinetic parameters are use to
calculate a new dose and dosing interval

 τ =¿[lnCpmax(ss) – lnCpmin(ss) / K]
= ln30-ln7 / 0.048
= 30h rounded to 36h

 D = cpss.max Vd (1 – e-kƮ )
= 30/60 (1-e-(0.048)(36) )
=1,480mg rounded to 1500mg

 The new dose of vancomycin is 1500mg every 36h (infused over 1h).
ACTIVITY NO 12
TO CONSTRUCT SOAP AND FARM NOTE ACCORDING TO THE CASE GIVEN.

CASE:
HISTORY OF PRESENT ILLNESS:-
Geraldine Johns is a 70-year-old woman seen Monday morning in clinic for her first visit. She
has just moved to town to be near her son following the death of her husband. She has a
history of atrial fibrillation, type 2 diabetes, COPD, mild heart failure, and is SIP MI 4 years ago.
She lives alone and maintains a good level of activity and self-care Denies pain in legs upon
walking. She is maintained on metformin 500 mg po BID, glyburide 10 mg po Q AM, famotidine
20 mg po daily, digoxin 0.125 mg po Q AM, warfarin 5 mg po Q AM, aspirin 81 mg po Q AM,
furosemide 80 mg po BID, and metoprolol XL 100 mg po Q AM.

PHYSICAL EXAMINATION:

 VITAL SIGNS:-
 B/P 169/88, P 68 and regular, RR 13, T 990 F; Wt 100 lbs, Ht 5'2"
 SKIN
 No rashes
 CARDIAC
 No murmurs or rubs. (+) S3 gallop; PMI in the 6th intercostal space 3 cm distal to the
midclavicular line
 CHEST
 Slight crackles at the right and left bases; no rales, e-to-a changes or tactile fremitus
 Ext
 1—2+ pedal edema bilaterally. ABI (ankle brachial index) = 1.02(negative)
 HEENT
 Slight AV nicking, otherwise unremarkable
 GI, GU and NEURO
 Unremarkable
 Laboratory Values Are Unremarkable with the Following Exceptions
 INR 3.5 Glucose 198 mg/dL
 AIC 11.3%
 Serum creatinine 1.3 mg/dL
 Digoxin level 1.0 ng/mL
 CHEST X-RAY
 Some diffuse patchiness at the bases. Enlarged cardiac silhouette. Decreased density of
the vertebrae consistent with mild osteoporosis.
 ECG
 Normal sinus rhythm
MEDICAL ASSESSMENT
l. Mild to moderate heart failure with pedal edema and slight pulmonary edema on digoxin and
metoprolol

2. Type 2 DIM, not optimally controlled on metformin and glyburide

3. Hypertension not optimally managed on metoprolol and furosemide

4. Atrial fibrillation, currently controlled on digoxin and metoprolol

5. Possible moderate renal insufficiency; Scr 1.3, estimated CLcr


=28 mL/min (Cockcroft & Gault)

6. Possible dyslipidemia, as suggested by history of MI

7. Osteoporosis suggested by chest radiographs

8. COPD requiring no additional intervention at this time

9. S/P MI, on aspirin; lipid status unknown.

CONSTRUCTION OF A SOAP OR FARM NOTE

Note: The Subjective and Objective findings of the SOAP note are combined into Findings for a
FARM note. The Plan of the SOAP note is split into Recommendations/Resolution and
Monitoring/Follow-Up in the FARM note.

FINDINGS

SUBJECTIVE: 70-year-old woman recently moved here after the death of her husband. Patient
complains of slight shortness of breath when walking up stairs and long distances. She voices
no other complaints. She has a history of atrial fibrillation, type 2 diabetes, COPD, mild heart
failure, and is SIP MI 4 years ago. She lives alone and maintains a good level of activity and self
care. She is maintained on metformin 500 mg po BID, glyburide 10 mg po Q AM, famotidine 20
mg po daily, digoxin 0.125 mg po Q AM, warfarin 5 mg po Q AM, aspirin 81 mg po Q AM,
furosemide 80 mg po BID, and metoprolol XL 100 mg po Q AM. She states that she takes her
medications as prescribed, but she has some difficulty describing precisely how she takes them
and is not quite certain what each medication does for her.

OBJECTIVE:

 VS: BP 169/88, P 68 and regular, RR 13, T 990F; wt 100 1b, Ht 5'2"


 CARDIAC: S3 gallop, PMI in the 6th intercostal space 3 cm distal to the midclavicular line
 CHEST: Slight crackles at the right and left bases
 EXTREMITIES: 1—2+ pedal edema bilaterally, ABI negative
 HEENT: Slight AV nicking, otherwise unremarkable
 MEDICATIONS:
 Metformin 500 mg po BID Glyburide 10 mg po Q AM
 Famotidine 20 mg po daily
 Digoxin 0.125 mg po Q AM
 Warfarin 5 mg po Q AM
 Aspirin 81 mg po Q AM
 Furosemide 80 mg po BID
 Metoprolol XL 100 mg po Q AM
 LABS:
 INR 3.5
 Glucose 198 mg/dL
 A1c 11.3%
 Serum creatinine 1.3 mg/dL
 Serum digoxin level 1.0 ng/mL
 Chest X-Ray: Some diffuse patchiness at the bases. Enlarged cardiac silhouette.
Decreased density of the vertebrae consistent with mild osteoporosis.
 ECG: NSR
ASSESSMENT

1. Possible non-adherence/concordance and lack of knowledge about medications.


2. Mild to moderate heart failure as suggested by pedal edema, DOE, and cardiomegaly on
chest x-ray. Maintained on a β-blocker and is not currently prescribed an ACE inhibitor.

3. Type 2 diabetes mellitus, not optimally controlled on metformin and glyburide; AIC above
goal of Not prescribed either an ACE inhibitor or an ARB for renal protective effects.

4. Hypertension, not optimally controlled on metoprolol, as suggested by increased BP,


elevated serum creatinine, and AV nicking. The renal and ophthalmic findings are suggestive of
significant, sustained hypertension. Repeated measurements will be necessary to confirm this
assessment.

5. Atrial fibrillation

 Rate control: Rate currently under control with metoprolol and digoxin. No adjustment
indicated.
 Anticoagulation: INR above target range of 2.0—3.0, without clinical complications at
this time. No cause could be identified, although a change in diet associated with recent
life events is suspected.
6. Possible moderate renal insufficiency as indicated by increased S Cr Renal dose adjustments
may be necessary.

7. SIP MI on aspirin.

8. Possible dyslipidemia as suggested by history of MI.

9. R/O osteoporosis: Chest radiography suggestive of osteoporosis. Her petite frame and age
are consistent with postmenopausal osteoporosis.

10. COPD: Mild DOE may suggest that the COPD is contributing to the heart failure symptoms.
COPT) appears to be an untreated indication.

11. Adverse medication effects: Although metoprolol may be considered appropriate for both
the post-MI and CHF indications and is a Pi-selective ß-blocker, its ß2-blocking properties
(usually at higher doses) may contribute to worsening COPD and/ or CHF due to
bronchoconstriction, negative inotropic effects, or both.
12. Medication without indication (famotidine): On further questioning, the patient recalls
being started on it while hospitalized for Ml 4 years ago, She was given a prescription for it
when she left the hospital. She has no complaints related to GERI) or PUD. No need for
famotidine can be identified.

PLAN (RECOMMENDATIONS/RESOLUTION)

1. Assess and reinforce adherence/concordance with recommended therapy. Educate on


purpose of each medication.

2. Mild to moderate heart failure: Continue both the ß-blocker metoprolol and digoxin,
pending evaluation by the Cardiology Service to determine appropriateness. Suggest initiation
of an ACE inhibitor at low doses and increasing furosemide to 100 mg po BID until her return
next week because of persistent pedal and pulmonary edema. No added dietary salt. May
consider adding spironolactone at next visit.

3. Type 2 diabetes mellitus:

 Medication: Suggest initiation of an ACEI (as above) per current ADA guidelines. Suggest
changing glyburide 10 mg to glipizide XL 10 mg po daily to improve control and enhance
compliance/concordance. Continue to follow blood glucose readings and, if indicated,
may supplement glyburide with insulin lispro for elevated pre-meal BG, based upon an
estimated insulin sensitivity of I unit per 30 to 40 mg/dL.

IF BLOOD GLUCOSE Give Insulin Lispro:

180mg/dL 2 units

220 3 units

260 4 units

300 5 units

340 6 units, and test for urinary ketones. Call PCP if


ketones are moderate or large.
 Diet: Suggest 3 meals and bedtime snack, with no concentrated carbohydrate (CHO)
choices. Limit CHO intake per meal to 60 g; snacks 15—20 g CHO. No added salt. Check
blood glucose AC and HS.
4. Hypertension: Suggest initiation of an ACEI (as above), started at low doses. If repeated
measurements confirm the diagnosis of hypertension, they may be titrated to maintain blood
pressure control. Blood pressure goal is < 130/80 mm Hg in patients with diabetes. Currently,
the patient is stage 2, è160/ 100 mm Hg.

5. Atrial fibrillation:

 Rate control: Suggest continuing metoprolol and digoxin unless Cardiology suggests
otherwise. No adjustment indicated at this time.
 Anticoagulation: INR is above target range of 2.0—3.0. Recommend warfarin 2.5 mg
today and then resume 5 mg po daily; dose to be adjusted as needed to maintain INR
between 2.0 and 3.0,
6. Renal insufficiency: Suggest hydration regimen and repeat serum creatinine. No medication
dosage adjustments are indicated currently.

7. S/P MI: Recommend continuation of aspirin 81 mg po Q AM. Suggest initiation of ACEI/ARB


as noted above, and a statin (e.g., pravastatin 10 mg po at bedtime). Continue metoprolol, if
acceptable to Cardiology.

8. Possible dyslipidemia: Treat based upon lipid panel; goal LDL is <IOO mg/dL in patient with
existing CAD or diabetes; this patient has both.

9. Possible osteoporosis: If DXA scan Indicates osteoporosis, begin a bisphosphonate (e.g.,


alendronate 70 mg po weekly) and calcium 1,500 mg daily.

10. COPD: COPD appears to be an untreated indication. Suggest initiation of ipratropium 2 puffs
QID.

11. Adverse medication effects: As noted above, will await Cardiology opinion on need
for/appropriateness of P-blocker and digoxin to manage CHF.
12. Medication without indication: Suggest discontinuation of famotidine.
MONITORING/FOLLOW-UP

l. RTC in I week.

2. Prior to RTC:

a. Laboratory (slips given)

• Baseline electrolytes (K, Na, Ca, and Mg levels in light of unopposed furosemide therapy
of unknown duration and use of digoxin) today
• Serum creatinine today.
• Fasting lipid panel next week prior to RTC.
• INR next week prior to RTC
b. DXA scan. Patient referred to Jones Pharmacy.

c. Cardiology education. Appointment made with Dr. Welford's office.

3. Patient instructed to monitor blood glucose AC and HS and bring information on RTC.

4. Prescribed medication after this visit:

 Enalapril 5 mg po daily for CHF, hypertension, and type 2 DM


 Metformin 500 mg po BID for type 2 DM
 Glipizide XL 10 mg po daily for type 2 DM substituted for glyburide 10 mg po Q AM
 Lispro, as indicated e, Digoxin 0.125 mg po Q AM for CHF and rate control
 Furosemide 100 mg po BID for CHF
 Warfarin 5 mg po Q AM for SIP MI and CVA prevention
 Aspirin 81 mg po daily for SIP MI
 Metoprolol XL 100 mg po Q AM for SIP MI and rate control
 Pravastatin 10 mg po at bedtime for hyperlipidemia
 Ipratropium 2 puffs QID for COPD, and
 D/C Famotidine 20 mg po BID
ACTIVITY NO 13
TO STUDY CASEES RELATED TO CLINICAL TOXICOLOGY.

CASE STUDY #1
A 14-year-old female is brought to your emergency department by her parents after she admitted
to ingesting a total of ten, 250 milligram amoxicillin tablets four hours ago after an argument at
home that resulted in loss of her phone privileges. Her parents are concerned that she was trying
to kill herself. She denies any co-ingestion and has no symptoms. There are no other
prescription medications in the home.

 PMH: None.
 Physical Examination:
 T: 99°F
 HR: 100 bpm,
 RR: 16 breaths per minute ,
 bp:100/70 mm Hg
 General: The patient is tearful, but otherwise in no distress.

The remainder of the physical exam is completely normal.

QUESTIONS:

1. What testing, if any, should be obtained?

2. Should activated charcoal be administered?

3. Are there other treatments that should be considered?

GENERAL APPROACH TO TOXIC INGESTIONS:

1. Acetaminophen levels should be obtained in all cases of reported or suspected poisoning,


regardless of history and physical exam. Acetaminophen is readily available and patients can
initially present without signs or symptoms even with toxic levels. Dose history should not be
used to make management decisions because studies have found no correlation between the
amount of acetaminophen reportedly ingested and the serum concentration measured. The
patient’s four hour acetaminophen level in this patient was 85 ug/mL. A pregnancy test should
be performed in all females of childbearing age, as women may attempt suicide due to an
unwanted pregnancy.
The role of routine urine drug screening in the evaluation of patients presenting to the emergency
department with psychiatric-related complaints is controversial. ACEP’s Clinical Policy:
Critical Issues in the Diagnosis and Management of the
Adult Psychiatric Patient in the Emergency Department, published in January 2006, makes a
level C recommendation that routine urine screening for drugs of abuse in alert, awake,
cooperative patients does not affect ED management and need not be performed as part of the
ED assessment. Often, this testing is requested by the receiving psychiatric facility for admission
purposes, long-term care planning or diagnosis. In these cases, it may be reasonable to obtain
this testing in the emergency department; however this testing should not delay patient
evaluation or transfer. These recommendations relate to the management of adult psychiatric
patients; pediatric patients are excluded.

2. Previously, activated charcoal was not routinely recommended in treatment of ingestions that
occurred greater than one hour prior to presentation; however newer data regarding
acetaminophen ingestions suggests that the half-life of this drug in the stomach is markedly
increased in overdose settings and that there may be some therapeutic benefit to its
administration past the traditional one hour mark. Other circumstances that may warrant charcoal
administration past the one hour mark include massive overdoses, poisoning with sustained
release preparations and ingestion of agents that slow gastrointestinal motility. Or
acetaminophen, activated charcoal may offer some benefit when used up to four hours post
ingestion.

3. The patient does not require treatment with N-acetylcysteine because her four hour
acetaminophen level falls below the toxicity line on the Rumack-Matthew nomogram. Based on
recommendations from the American Academy of Clinical Toxicology, this patient does not
meet criteria for gastric lavage as she meets neither of two criteria for this intervention: ingestion
of a potentially life-threatening amount of a poison and presentation within 60 minutes of
ingestion. For similar reasons, this patient will not benefit from whole bowel irrigation. Home
administration of ipecac syrup is no longer recommended by the American Academy of
Pediatrics and its routine use in the emergency department is discouraged by the American
Academy of Clinical Toxicology.

CASE STUDY #2

A 40-year-old male presents to your emergency department after falling into a vat of chromic
acid. The patient arrives via EMS with a dry cough and is actively vomiting. He is complaining
of chest pain and shortness of breath.

 PMH:
 Asthma.
 Medications: Albuterol inhaler as needed.
 Physical Examination:
 T: 98.6°F
 HR: 115 bpm
 RR: 29 breaths per minute
 BP: 176/94 mm Hg
 General: He is awake and alert.
 HEENT:
 Normal.
 Pulmonary:
 Diffuse wheezing, poor air exchange.
 CV: Tachycardia, regular rhythm without murmur, normal perfusion. Extremities:
Diffuse skin ulcers in exposed areas.

QUESTIONS:

1. What would be your initial approach to this patient?

2. What complications may be associated with this type of exposure?


3. What therapy is indicated?

GENERAL APPROACHES FOR CHROMIC ACID EXPOSURE


1. Decontamination should accompany stabilization of the airway, breathing and circulation. The
patient should have all clothing removed and copious aqueous irrigation performed.
2. Chromic acid is a strong acid that contains the hexavalent (CrVI 3), or most hazardous, form of
chromium. Acute skin exposure may cause burns and chronic exposure may result in skin and
nasal ulcer formation. These skin ulcers are round or oval growths with reddish edges and
necrotic centers and are often referred to as “chrome holes” or “chrome sores”. Chromic acid
inhalation may be associated with upper respiratory irritation and bronchospasm, manifested by
cough, chest pain and dyspnea. Pulmonary congestion visible on radiographs, interstitial
pneumonia and delayed, non-cardiogenic edema have been reported. Systemic effects include
renal failure secondary to acute renal tubular acidosis, hemolysis and liver damage.
3. Initially, the focus should be decontamination, including removal of contaminated clothing
and a deluge, or heavy downpour safety shower. Fluid and electrolyte balance should be
maintained, especially in the case of large skin and mucosal lesions which can lead to significant
fluid losses. The efficacy of activated charcoal has not been demonstrated. Ascorbic acid
(vitamin C) has been recommended for cases of ingestion and skin exposure to reduce absorption
of chromium by oxidizing it from the hexavalent to trivalent form, which does not cross cell
membranes as rapidly. This intervention must be performed within two hours of exposure. Beta
agonist therapy is indicated for bronchospasm. Patients should be observed for the development
of renal failure, non-cardiogenic pulmonary edema and liver failure. Hemodialysis, exchange
transfusion and chelation therapy are ineffective.
The Poison Control Center should be called for advice on antidotes and for assistance with
management of poisoning/exposure to unfamiliar chemicals.
Prevention of exposure to chromium, particularly respiratory exposure, is critical as chromium
has a demonstrated carcinogenic potential.

CASE STUDY #3
A 30-year-old white male presents to your emergency department after ingesting “white
powder” from a bag that was given to him by his friend. He has developed weakness, vomiting
and diarrhea.

 PMH:
 None.
 Physical Examination:
 T: 100.4°F
 HR: 120 bpm
 RR: 20 breaths per minute
 BP: 90/60 mm Hg
 General:
 He is awake and alert, but actively vomiting and having diarrhea.
 Pulmonary:
 Clear to auscultation.
 CV:
 Tachycardic without murmur, normal perfusion.
 Neurologic:
 GCS 15. Cranial nerves II-XII intact.
 Remaining neurologic exam is nonfocal.

QUESTIONS:
1. From what type of poisoning is this patient suffering and what are the typical signs and
symptoms?
2. What initial therapy, if any, should be instituted?
GENERAL APPROACHES:
1. This patient is suffering from arsenic poisoning. Arsenic is a naturally occurring metalloid
element. Acute poisoning predominantly affects the gastrointestinal system, causing nausea,
vomiting, abdominal pain and diarrhea. Affected individuals may have a garlic odor to their
breath or stool. Resultant dehydration heralds cardiovascular instability, which occurs rapidly
and progresses from sinus tachycardia to orthostatic hypotension with possible shock and death,
depending on the amount and form of arsenic ingested. Patients may develop severe
encephalopathy with delirium, confusion, seizures and coma. Other acute complications include
rhabdomyolysis and acute renal failure.
Although a symmetrical sensorimotor peripheral polyneuropathy may develop 1-3 weeks
following ingestion, some patients may develop symptoms within 24 hours. Sensory symptoms
usually occur first with patients complaining of “pins and needles” or electrical shock-like pains
in the lower extremities. Early examination may demonstrate isolated, diminished or absent
vibratory sense. Motor weakness may later develop and can sometimes mimic Guillain-Barré
syndrome. Reversible pancytopenia and hepatitis can occur within one week after the initial
illness. Dermatologic lesions, a dry, hacking cough and Mees lines (horizontal 1-2 mm white
lines on the nails) can also develop after severe acute and chronic exposures.
2. The white powder was rapidly identified as arsenic and a spot urine arsenic level was sent for
confirmation of ingestion. Blood and urine were sent to the lab for determination of arsenic
levels. Acute arsenic toxicity is life threatening and necessitates aggressive treatment.
Initial management should be focused on stabilizing the airway, breathing and circulation. The
patient should receive 2 large bore IV’s and be placed on a cardiac monitor with continuous
pulse oximetry. Hypotension should be treated with crystalloid fluids; however, pressor agents
may be required. Fluid status should be carefully monitored, as cerebral and pulmonary edema
may occur. Potassium, calcium and magnesium concentrations should be maintained in the
normal range and urine output should be maintained. Ventricular dysrhythmias may occur.
Ventricular tachycardia and ventricular fibrillation are treated with lidocaine and electrical
defibrillation. Because arsenic is associated with prolongation of the QTc, agents that prolong
the QTc should be avoided (class IA, IC and III antidysrhythmic agents). Bicarbonate therapy
may be effective.
Chelation therapy should be initiated as soon as possible with Unithiol (DMPS, a water-soluble
analog of dimercaperol), dimercaperol (BAL, second choice if unithiol not immediately
available) or DMSA (oral succimer), under the direction of a medical toxicologist.
Activated charcoal is sometimes used for ingestions that present within one hour, but its efficacy
has not been proven.

CASE STUDY 4
A 12-month-old male presents to your emergency department after ingesting a watch battery,
which was left out on the counter. He has been drooling since the incident and refusing his
bottle.
 PMH:
 None.
 Physical Examination:
 T: 98.6°F
 HR: 137 bpm
 RR: 32 breaths per minute
 BP: 100/62 mm Hg
 General:
 He is awake, alert and calm in appearance.
 HEENT:
 Drooling from mouth.
 Pulmonary:
 Clear to auscultation.
 CV:
 Regular rate and rhythm without murmur, normal perfusion. Extremities: Normal.

QUESTIONS:-
1. What is the initial approach to this patient?
2. What complications may be associated with these types of batteries?
3. On x-ray, the battery is located in the esophagus at the level of the aortic arch. What therapy is
indicated?
GENERAL APPROACHES FOR BUTTON BATTERY INGESTION
1. Any patient presenting with possible foreign body ingestion should have a complete
assessment of his airway and respiratory status, including pulse oximetry readings when
indicated. The child should remain in the upright position and NPO. Both anteroposterior and
lateral radiographs should be obtained, imaging from the nasopharynx to the anus to localize the
position of the foreign body. 2. Complications may occur for several reasons, including electrical
discharge, pressure necrosis, obstruction and leakage of battery contents. Electrical discharge is
the most important mechanism in most clinically significant cases. Discharged batteries still
retain enough voltage and storage capability to generate an external current; however newer
batteries are associated with a greater potential for tissue damage. The larger the battery the
more likely an esophageal obstruction will occur. Esophageal perforation and aspiration have
also been reported. In the majority of cases, 89% in one series, the battery will pass
spontaneously without complication. Systemic absorption of heavy metals from broken
or fragmented batteries is a common concern but has been rarely reported. Mercury batteries
may pose a particular hazard if they break.
3. This battery requires emergent removal because of its location in the esophagus. Esophageal
injury from button batteries has been reported in less than two hours. Endoscopy is the removal
method of choice. Foley catheters have been recommended for removal of esophageal foreign
bodies, but their use carries an added risk of aspiration. Magnetized probes are an alternative in
skilled hands. Risks are lower after entry into stomach but not absent. For button batteries in the
stomach, monitoring of stool content or follow up x-ray in one week is recommended. Parents
should be educated about concerning symptoms, including abdominal pain and vomiting.

CASE STUDY #5
A 19-month-old male presents to your emergency department with his parents after ingesting 35
mL of phenytoin suspension. Parents relate that he appears to be “wobbly” and “sleepy”. He
has had no vomiting and no seizure activity.

 PMH:
 Brain aneurysm,
 seizure disorder,
 feeding disorder.
 Physical Examination:
 T: 100.4°F
 HR: 132 bpm
 RR: 30 breaths per minute
 BP: 110/70 mm Hg
 General:
 He appears very sleepy but is arousable and has an intact gag reflex.
 HEENT:
 Examination reveals horizontal and vertical nystagmus.
 Mouth examination reveals gingival hyperplasia.
 Pulmonary:
 Clear to auscultation.
 CV:
 Regular rate and rhythm without murmur, capillary refill normal.
 Neurologic:
 GCS = 15, cranial nerves II-XII intact.
 Truncal ataxia is present.
 Hyperreflexia present, all DTR’s.
QUESTIONS:
1. What are the usual signs of acute phenytoin toxicity?
2. What initial therapy should be instituted?
3. What are the signs and symptoms of chronic phenytoin toxicity?
GENERAL APPROACHES FOR PHENYTOIN POISONING
1. CNS effects are the most common symptoms of acute phenytoin ingestion. The minimum oral
toxic dose is 20 mg/kg. Mild to moderate intoxication causes horizontal nystagmus, ataxia,
ophthalmoplegia, dysarthria, hyperreflexia, hyperglycemia, irritability and altered mental status.
Severe intoxication causes stupor, coma and respiratory arrest. While phenytoin toxicity can
produce paradoxical seizures, this finding should prompt a search for other causes as this is a
rare finding. Death from phenytoin poisoning is also rare.
Serum phenytoin levels can be obtained and it is generally recommended that repeated levels are
determined because of potential for slowed absorption. The therapeutic range is 10-20 mg/L. At
levels under 10 mg/L, systemic manifestations are rare. t levels 10-20 mg/L, mild nystagmus
may be present. At levels between 20-30 mg/L nystagmus is common, and ataxia may occur. At
levels between 30-40 mg/L patients often develop ataxia and slurred speech. At levels between
40-50 mg/L patients may develop lethargy, confusion and combativeness. At levels above 50
mg/L patients also develop choreoathetoid movements and opisthotonic posturing. Survival has
been reported in three patients with levels greater than 100 mg/L. Although cardiovascular
effects occur after rapid intravenous administration of phenytoin, due to the propylene glycol
excipient, these effects do not occur after chronic or acute oral exposures
In some instances, the patient's serum phenytoin level may seem discordant with their
symptoms. In these situations, a serum albumin level might be helpful as higher free phenytoin
concentrations are seen in the setting of hypoalbuminemia. Because it is the free phenytoin
concentration that determines toxicity, but the total level that is reported, hypoalbuminemic
patients may exhibit significant symptoms in the setting of only mildly elevated levels. Free
phenytoin concentrations can be obtained; however they are generally not measured unless there
is clinical uncertainty of the diagnosis.
2. Initial management is focused on stabilizing the airway, breathing and circulation.
Patients with ataxia should have precautions taken to prevent injury from fall. Since the child
has a seizure disorder, it is important not to drop the anticonvulsant level to a sub therapeutic
range. If seizures occur, treat in the usual way and search for other causes. In the appropriate
situation, activated charcoal may be administered. If the level is very high and the patient has
significant symptoms, multi-dose activated charcoal can be given to enhance phenytoin
elimination but is not necessary and may increase aspiration risk in symptomatic patients.
Physicians should weigh the benefits of multidose activated charcoal in patients in need of
chronic phenytoin therapy for seizure control.
3. Patients on long term phenytoin therapy can develop gingival hyperplasia, which is the most
common adverse effect in adults and children. Chronic phenytoin
toxicity may result in phenytoin encephalopathy. Other adverse effects include hyperglycemia
secondary to impaired insulin secretion, hypothyroidism, osteomalacia, aplastic anemia,
malignant lymphoma, hemorrhagic disease of the newborn (responsive to vitamin K), and
megaloblastic anemia secondary to decreased folate absorption and altered folate metabolism
(responsive to folic acid).

CASE STUDY #6
A 19-year-old female presents to your emergency department after ingesting a large amount of
rubbing alcohol following a fight with her boyfriend. She appears very sleepy and complains of
generalized weakness. She now denies suicidal ideation and has no plan to injure herself. She
denies any co-ingestion and the paramedics found no other pills or substances in the house.
 PMH:
 None.
 SH:
 No previous suicide attempts or history of depression.
 Physical Examination:
 T: 99.4°F
 HR: 78 bpm
 RR: 18 breaths per minute
 BP: 90/60 mm Hg
 General:
 Lethargic.
 HEENT:
 Acetone odor on the breath, otherwise normal.
 Pulmonary:
 Clear to auscultation.
 CV:
 Regular rate and rhythm without murmur, capillary refill 4 seconds.
 Neurologic:
 GCS 14. Cranial nerves II-XII intact.
 Ataxia is present.
 All deep tendon reflexes are depressed.
 Strength is 3/5 all flexors and extensors of bilateral upper and lower extremities.
QUESTIONS
1. What substance did the patient ingest?
2. What are the usual signs of acute toxicity?
3. What initial therapy should be instituted?
4. What are the characteristic laboratory findings?

GENERAL APPROACHES TO ISOPROPANOL POISONING


1. This patient ingested isopropyl alcohol. Rubbing alcohol contains approximately 70%
isopropanol. It is also found in solvents, antifreeze and disinfectants. The primary reason people
ingest this substance is to become intoxicated (for instance, as an inexpensive ethanol substitute
in alcoholics) or to harm themselves.
2. The major effects of acute isopropanol ingestion are on the central nervous system, mimicking
the inebriation caused by ethanol, and gastrointestinal systems. The usual signs and symptoms
include CNS depression, slurred speech, ataxia, lethargy, weakness, nausea and headache.
Abdominal pain, gastritis, hypotension and apnea can also occur. Uncommon adverse effects
include hemolytic anemia, hypothermia, renal tubular acidosis and rhabdomyolysis. Death from
isopropyl alcohol use is rare but can occur secondary to coma with untreated airway
compromise, injury resultant from ataxia or stupor, or rarely, hypotension caused by vasodilation
and possible myocardial depression after massive overdose. Some sources give an estimated
lethal dose of 250 mL in adults; however with treatment, adults and children have survived much
larger ingestions.
3. Initial management should be focused on stabilizing the airway, breathing and circulation. If
exposure is by the cutaneous route, skin decontamination should be extensive as significant
absorption and toxicity can occur, especially in infants. It is important to ensure that no methanol
or ethylene glycol were coingested. Serum isopropanol levels are mostly used to substantiate the
diagnosis and treatment is supportive. Levels greater than 100 mg/dL can cause a decreased level
of consciousness. This patient requires intravenous access and volume resuscitation.
Hypoglycemia should be corrected. There is no role for gastrointestinal decontamination due to
rapid absorption and favorable outcomes with supportive care alone. Active charcoal can adsorb
isopropyl alcohol; however massive doses must be used and are impractical given the fact that
most patients will have CNS depression and recover with supportive care alone. Rarely,
hemodialysis is needed for massive ingestions. It effectively removes isopropyl alcohol and
acetone from the circulation. Indications for hemodialysis include isopropanol levels exceeding
400-500 mg/dL, renal failure, hypotension and coma in patients unresponsive to supportive care
(intravenous fluids or vasopressors). Since the primary metabolite (acetone) is less toxic than the
parent compound, there is no indication for ADH inhibition with fomepizole or ethanol.
4. It is crucial to differentiate isopropyl alcohol poisoning from that of ethylene glycol or
methanol, as the latter are more dangerous. Characteristic laboratory findings include
euglycemia, ketosis, little or no acidosis and increased osmolality. Isopropanol is metabolized by
alcohol dehydrogenase to acetone, which can worsen CNS depressant effects and accounts for
the marked ketosis seen in these patients. Isopropanol can be distinguished from methanol and
ethylene glycol because it does not produce an elevated anion gap metabolic acidosis.
CASE STUDY #7
A 17-year-old male presents to your emergency department after accidentally ingesting a large
amount of methanol because he thought it was Gatorade®. He is not suicidal. He denies any co-
ingestion, and the paramedics did not find any pills or substances in the house. The ingestion
occurred approximately four hours prior to the call to EMS. He is currently complaining of
blurred vision and nausea.
 PMH:
 None.
 SH:
 No previous suicide attempts or history of depression.
 Physical Examination:
 T: 99.4°F
 HR: 120 bpm
 RR: 24 breaths per minute
 BP: 110/60 mm Hg
 General:
 He is awake and alert.
 HEENT:
 Examination reveals dilated pupils with sluggish light reaction and poor accommodation.
 Pulmonary:
 Clear to auscultation.
 CV:
 Regular rate and rhythm without murmur,
 capillary refill slightly prolonged.
 Neurologic:
 GCS = 14.
 Cranial nerves II-XII intact.
QUESTIONS
1. What are the usual signs of acute toxicity?
2. Which initial therapies should be instituted?
3. What are the characteristic laboratory findings?
GENERAL APPROACHES FOR METHAMOL POISONING
1. Methanol can be found in multiple industrial products, including antifreeze, solvents,
disinfectants, de-icing solutions, windshield wiper fluid, and fuels. Exposure by ingestion is
associated with the most negative effects, while cutaneous and inhalational exposures rarely
cause toxicity. The primary reason people ingest this substance is to become intoxicated (for
instance, as an ethanol substitute in alcoholics) or to harm themselves. Accidental poisonings can
occur and affect multiple people in the setting of improper distillation of moonshine. The initial
effects of methanol are inebriation and gastrointestinal discomfort. Due to metabolism of the
parent alcohol to formic acid, a potent and specific neurotoxin, patients develop edema of the
optic nerve with resultant visual changes, and ultimately, permanent blindness. Ischemic or
hemorrhagic injury to the basal ganglia has been reported. Seizures, coma and death are possible.
An afferent papillary defect is an ominous sign in methanol poisoning. A funduscopic exam may
reveal disc hyperemia and papilledema.
2. Initial management should be focused on stabilizing the airway, breathing and circulation.
Methanol itself is of limited toxicity, but its metabolites produce toxicity. If methanol exposure is
suspected, a stat blood level should be obtained. In any patient who has ingested more than a sip,
has a metabolic acidosis and/or an osmolal gap, ADH inhibiting therapy with ethanol or
fomepizole should be started immediately. The agent of choice is generally institution specific
but a knowledge of each is important.
Ethanol, in sufficient concentrations, (greater than 100 mg/dL), competitively inhibits the
formation of the toxic metabolites, as it has a greater affinity for ADH than methanol. This
allows the unchanged parent alcohol (methanol) to be excreted by the pulmonary and renal
routes. The loading dose is 15 ml/kg of 5% ethanol followed by a maintenance infusion of 2-4
ml/kg/hr. Ideally, the blood ethanol level should be maintained between 100-150 mg/dL.
Treatment can be discontinued when methanol levels are below 20 mg/dL.
Fomepizole also has higher affinity for alcohol dehydrogenase than methanol and as such acts
similar to ethanol to prevent the formation of toxic metabolites. It is becoming the antidote of
choice in most institutions. Fomepizole is administered as follows: 15 mg/kg IV loading dose
over 30 minutes, followed by maintainence doses. Maintainence doses are administered as
follows: 10 mg/kg IV q12h for 48 hours, then 15 mg/kg IV q12h until methanol level is < 20
mg/dL. The acid-base status must be followed carefully and bicarbonate therapy may be
required. After ADH blocking therapy, the elimination of methanol via the pulmonary and renal
routes becomes first order and is drastically slowed (t 1/2 of approx 48 - 54 hours). Because of
this, non-emergent hemodialysis is generally performed to remove methanol and avoid the
excess cost associated with prolonged hospital stays and prolonged use of ADH inhibitors.
Cofactor therapy with folic acid is sometimes used to expedite elimination of formic acid, which
is
partially dependent on tetrahydrofolate.
3. Characteristic laboratory findings include an elevated anion gap metabolic acidosis and an
osmolal gap.

CASE STUDY #8
An 18-year-old male presents to your emergency department after ingesting an unknown
quantity of lysergic acid diethylamide (LSD). His friends brought him in because he was “acting
goofy.” He is not currently suicidal and has no plan to hurt himself. He claims not to have taken
any other substances.
 PMH:
 None.
 SH:
 No previous suicide attempts and no history of depression.
 Physical Examination:
 T: 100.4°F
 HR: 124 bpm
 RR: 18 breaths per minute
 BP: 150/90 mm Hg
 General:
 Agitated and actively hallucinating.
 The skin is moist and pale.
 HEENT:
 Pupils are 4 mm bilaterally with sluggish light reaction. No nystagmus
 Pulmonary:
 Clear to auscultation.
 CV:
 Regular rate and rhythm without murmur.
 Abdomen:
 Soft and nontender with hyperactive bowel sounds.
 Neurologic:
 GCS 14.
 Cranial nerves II-XII intact.
 Fine tremor.
QUESTIONS
1. What are the usual signs of acute toxicity?
2. How is the diagnosis confirmed and which initial therapy should be instituted?
3. What are the characteristic laboratory findings?
GENERAL APPROACHES TO LSD POISONING
Lysergic acid diethylamine (LSD) and similar hallucinogens are known by some as "enactogens"
(to touch within). Despite much research, the exact mechanism of action is unknown. The major
effects from an acute LSD ingestion include hallucinations and mild sympathetic effects.
1. The usual sympathetic signs include hypertension, tachycardia, hyperthermia, mydriasis,
bruxism, diaphoresis, tremor and decreased attention span, which, similar to hallucinations, seem
to be doserelated. Paranoia and panic can occur at any dose. The toxic dose is variable and might
be only slightly greater than the recreational dose. The desired enactogenic effects generally do
not increase with increasing doses. Psychedelic agents rarely produce life-threatening problems.
Morbidity and mortality from LSD are extremely rare and result from associated trauma or from
intense sympathomimetic stimluation, including severe hyperthermia, seizure, intracranial
hemorrhage, cardiac arrhythmias, rhabdomyolysis and myoglobinuria, renal failure, hepatic
necrosis and disseminated intravascular coagulopathy.

2. The diagnosis is made by history and physical examination. Specific drug levels are not
widely available or useful in the emergency department. Amphetamine derivatives in this class
may cross-react with urine toxicology screening for amphetamines; however LSD and other non-
amphetamine hallucinogens will not be reported on urine toxicology screens. Initial management
should focus on stabilizing the airway, breathing and circulation. Supportive care is usually all
that is required. Even if a psychedelic agent is suspected, the patient with altered mental status
should receive dextrose, oxygen, thiamine and, if respiratory depression, naloxone. As always,
other etiologies must also be considered in the differential diagnosis. The patient should
optimally be placed in a quiet, but wellobserved location with minimal stimuli and a calm
support person. Reassurance and parenteral administration of benzodiazepines will usually
adequately treat patients having a "bad trip" (i.e. who are fearful, crying, paranoid) and those
with agitation, dysphoria and the signs of sympathetic excess. Hyperthermia must be
aggressively treated with hydration, active external cooling and muscle relaxants ranging from
benzodiazepines to paralytic agents, depending on the severity.
3. The laboratory findings are usually normal. CPK and urine should be obtained in patients with
severe signs and symptoms to rule out rhabdomyolysis and myoglobinuria.

CASE STUDY #9
A 17 month old male presents to your emergency department with his parents after he was
found eating small pellets in the neighbors’ basement. The child is asymptomatic. The patient’s
mother thinks the product is “some kind of super rat killer”.
 PMH:
 None.
 Physical Examination:
 T: 99.4°F
 HR: 110 bpm
 RR: 18 breaths per minute
 BP: 90/40 mmHg
 General:
 Alert male in no acute distress.

 HEENT:
 No pellet fragments in mouth. Handling secretions.
 Pulmonary:
 Clear to auscultation.
 CV:
 Regular rate and rhythm without murmur.
 Abdomen:
 Soft, non tender.
 Neurologic:
 No focal deficits.
QUESTIONS
1. What type of chemical did this child ingest and what is its mechanism of action?
2. What are the usual signs of acute toxicity?

3. What initial therapy should be instituted?

4. What other chemicals are used as rodenticides?

GENERAL APPROACHES TO SUPERWARFARIN POISONING

1. The most common rodenticides available today are the “superwarfarins,” brodifacoum,

diphacinone, bromadiolone, chlorophancinone, difenacoum, pindone and valone. The most

common is brodifacoum. These substances have intense and long–lasting anticoagulant effects

and act by inhibiting the vitamin K dependent clotting factors (II, VII, IX, X) for weeks to

months. Because they look similar to oats and grain and have a sweet taste, children can mistake

them for food. Significant toxicity due to transcutaneous absorption of liquid preparations has

been reported.

2. Because peak effects do not occur for two to three days (owing to the long half lives of factors

IX and X), patients are usually asymptomatic after ingestion. Chronic use or delayed

presentation can be manifested with signs of easy bleeding (such as petechiae under a blood

pressure cuff, mucosal bleeding, hematuria), but can rarely present with more severe, potentially

life-threatening bleeding.
3. Usually no initial treatment or laboratory tests are required after accidental pediatric

ingestion. Vitamin K should not be administered, as it will make determination of toxicity

impossible. Unless the child has underlying disease or abnormal clotting, baseline coagulation

studies are not required. However, the child should be referred for daily prothrombin time

values for three days. If they remain normal, no other treatment is required. In adult populations,

baseline coagulation studies, CBC, type and cross could be considered depending on the clinical

situation. A normal PT/INR 48 hours after ingestion excludes clinically significant ingestion.

Commercially available Brodifacoum levels can be obtained at two laboratories in the United

States and are mainly useful to diagnose repeated ingestions in patients whose PT/INR is failing

to decrease appropriately, or is increasing despite oral vitamin K therapy (as sometimes seen in

patients with underlying psychiatric issues).

4. One newer agent that has emerged as a potentially dangerous rodenticide is bromethalin,

which was developed to combat increasing resisitance of rats to the superwarfarins. This

rodenticide acts as a potent and specific neurotoxin, uncoupling CNS mitochondrial oxidative

phosphorylation and ultimately leading to cerebral edema, elevated ICP, seizures, coma and

death. Multidose activated charcoal can be used to adsorb this toxicant. Other treatment

strategies include dexamethasone and mannitol (useful during the absorptive phase) and

supportive care. Other agents used in the past as rodenticides include zinc phosphide (still

available in the Southwestern US), red squill, strychnine, arsenic and thallium.
ACTIVITY NO 15
STEPWISE APPROACH TO START IV THERAPY AND CALCULATION OF
DRIP FLOW RATE AND MEDICATION INFUSION RATE

STEPWISE APPROACH TO INITIATE IV THERAPY:


1. Introduce yourself to the patient and clarify the patient’s identity. Explain the procedure to the
patient and gain informed consent to continue. Inform that cannulation may cause some
discomfort but that it will be short lived.
2. Ensure that you have all of your equipment ready as follows:
 Alcohol cleanser.
 Gloves.
 An alcohol wipe.
 A disposable tourniquet.
 An IV cannula.
 A suitable plaster.
 A syringe.
 Saline.
 A clinical waste bin.
3. Sanitize your hands using alcohol cleanser
4. Position the arm so that it is comfortable for the patient and identify a vein.

5. Apply the tourniquet and re-check the vein.

6. Put on your gloves, clean the patient’s skin with the alcohol wipe and let it dry.

7. Remove the cannula from its packaging and remove the needle cover ensuring not to touch
the needle.
8. Stretch the skin distally and inform the patient that they should expect a sharp scratch.
9. Insert the needle, bevel upwards at about 30 degrees. Advance the needle until a flashback of
blood is seen in the hub at the back of the cannula
10. The flashback of blood is seen, progress the entire cannula a further 2mm, then fix the
needle, advancing the rest of the cannula into the vein.

11. Release the tourniquet, apply pressure to the vein at the tip of the cannula and remove the
needle fully. Remove the cap from the needle and put this on the end of the cannula.

12. Carefully dispose of the needle into the sharps bin.

13. Apply the dressing to the cannula to fix it in place and ensure that the date sticker has been
completed and applied.

14. Check that the use-by date on the saline has not passed. If the date is ok, fill the syringe with
saline and flush it through the cannula to check for patency.

15. If there is any resistance, or if it causes any pain, or you notice any localized tissue swelling:
immediately stop flushing, remove the cannula and start again.

16. Dispose of your gloves and equipment in the clinical waste bin, ensure the patient is
comfortable and thank them

WHEN INITIATING OR CHANGING AN IV BAG OF FLUIDS OR MEDICATIONS, IT


IS IMPORTANT TO REMEMBER THESE ITEMS:

 IV fluids are a medication. Verify physician orders and check that the patient does not have an
allergy to this medication. Perform the six rights of medication administration three times as you
would when giving any other medication. Check the type of fluid and the expiration date, and
verify the fluid is free of discoloration and sediment. Check the expiration date when obtaining a
new tubing administration set.
 Examine the bag to ensure that the bag itself is intact and not leaking. There may be moisture on
the inside of the plastic IV bag storage container; this is normal.
 Verify the infusion rate of IV fluids is appropriate based on the patient’s age, size, preexisting
medical conditions, and prescribed indication. If a manual calculation is needed to set the
IV flow rate, calculate the rate and double-check the calculated rate with another registered
nurse.
 IV tubing administration sets require routine replacement to prevent infection. Follow agency
policy regarding initiating tubing change before initiating a new bag of fluid or medications.
 If administration set tubing is present, trace the tubing from the patient to its point of origin to
make sure that you’re accessing the correct port.
 Assess the IV site. Inspect for redness, swelling, or tenderness that can be a sign of irritation,
inflammation, or infection.
 Ensure the IV site is patent when initiating new fluid or medication. Aspirate for blood return
and flush the IV catheter according to agency policy.

NUMERICAL PROBLEM:-

Calculate the flow rate for 250ml of 0.5% dextrose to be administered over 3 hours.
If the infusion set has drop factor of 30drops/ml. calculate IV flow rate according to this.
SOLUTION:-
 Volume = 250ml
 Time = over 3 hours
 Drop factor = 30 drops/ml
 Time = 3 h or 180min
Volume × Drop
 Flow rate =
time
250
= ×20 (20 is Normal drop factor)
180
= 27.77 drops/min.
Volume
 Flow rate = × drop factor
time
250
= ×30
180
= 41.66 drops/min.
 Infusion rate = flow rate × concentration
=30 (drops/min or ml/min) ×0.5 (mg/ml)
=15mg/min
ACTIVITY NO 16

INTRODUCTION TO VAROIUS MEDICATION ADHERANCE MEASURING SCALES

Adherence Measuring Scales:


Medication nonadherence is a growing concern to healthcare systems, physicians and other
stakeholders because of mounting evidence that it is prevalent and associated with adverse
outcomes and higher costs of care. Patients with chronic diseases often receiving multiple
medications, are at higher risk for nonadherence to medication and medication adherence can be
essential for improving health outcomes. To date, measurement of patient medication adherence
and use of interventions to improve adherence is rare in clinical and pharmaceutical practice.
Physicians’ lack of knowledge and patients’ lack of awareness account for about 70% of non-
adherence, indicating the necessity to improve physician education, and patient involvement.
Medication Adherence Scales are tools and methods for measuring and evaluating; adherence
and compliance and medication taking behavior among patients. Among the various tools
developed over the past 40 years are the following:
 Neuroleptic Dysphoria Scale; NDS (Van Putten and May, 1978)
 Dysphoric Response Index; DRI (Singh and Kay, 1979)
 Drug Attitude Inventory; DAI (Hogan et al 1983; Awad, 1993)
 Medication Adherence Questionnaire; MAQ (Morisky et al, 1986)
 Rating of Medication Influences; ROMI (Weiden et al, 1994)
 Subjective Well-Being under Neuroleptic Treatment self-applied scale; SWN (Naber et
al, 1995; 2001)
 Clinician Rating Scale; CRS (Kemp et al, 1996, 1998) · Medication Adherence Rating
Scale; MARS (Thompson et al, 2000)
 Attitudes towards Neuroleptic Treatment; ANT (Kampman et al, 2000)
 Personal Evaluations of Transitions in Treatment; PETiT (Voruganti and Awad, 2002)
 Brief Evaluation of Medication Influences; BEMIB (Dolder et al, 2004)
 Brief Adherence Rating Scale; BARS (Byerly et al 2008)
 Drug Attitude Inventory (DAI) (Hogan et al, 1983)
 Personal Evaluations of Transitions in Treatment (PETiT) (Voruganti and Awad, 2002)
 Medication Adherence Rating Scale (MARS) (Thompson et al, 2000)
 Clinician Rating Scale (CRS) (Kemp et al, 1996; 1998)
 Brief Medication Questionnaire (BMQ) (Byerly et al 2008)
 Self-efficacy for Appropriate Medication Use (SEAMS)
 The Hill-Bone Compliance Scale
 Adherence to Refills and Medications Scale (ARMS)
 Adherence Scale Culig

1. Drug Attitude Inventory; DAI (Hogan et al, 1983):


The DAI consists of a questionnaire that is completed by the patient. It includes a series
of questions, each with true/false answers, pertaining to various aspects of the patient’s
perceptions and experiences of treatment. The original scale consists of 30 questions, but
a short form consisting of 10 questions has also been validated. The patient should be
asked to read each statement in the questionnaire and decide whether they believe it to be
true or false (or mostly true/false) as applied to their own experience with medications
(only those medications used for the patient’s mental health needs). They should circle
their answers in ink on the form.
SCORING: The DAI-30 contains 15 items that a patient who is fully adherent to their
prescribed medication (and so would be expected to have a ‘positive’ subjective response
to medication) would answer as ‘True’, and 15 items such a patient would answer as
‘False’. To calculate the score from a set of answers, each ‘positive’ answer is given a
score of plus one, and each ‘negative’ answer is given a score of minus one. In the
following table, the ‘positive’ answers (score = plus one) are shown in bold text. In
question one, for example, an answer of ‘False’ would score plus one and an answer of
‘True’ would score minus one. The total score for each patient is calculated as the sum of
the positive scores, minus the negative scores. A positive total score indicates a positive
subjective response (adherent) and a negative total score indicates a negative subjective
response (non-adherent)
CUTT-OFF: A positive total score indicates a positive subjective response (adherent)
and a negative total score indicates a negative subjective response (non-adherent).
2. Personal Evaluations of Transitions in Treatment; PETiT (Voruganti and Awad,
2002)
PETiT is another self-administered patient questionnaire. It was developed with the aim
of producing a tool that could monitor changes perceived by a patient receiving therapy
based on antipsychotic drugs, and particularly to measure the effects of atypical
antipsychotic drugs on outcomes such as subjective well-being. The patient should be
advised that the questions are about how they have been feeling and doing during the past
week. They should read each of the statements in the questionnaire and should choose the
answer that best indicates their feelings, by circling it with a pen. They should use the
following key:
Often - Frequently feel or act in the way described
Sometimes - Only feel or act that way occasionally
Never - Had not felt or acted that way during the past week
3. Medication Adherence Rating Scale; MARS (Thompson et al, 2000)
Thompson et al (2000) identified several deficiencies in the DAI as a measure of
adherence and proposed a new inventory, the MARS scale, that incorporates features of
both the DAI and the MAQ (Morisky et al, 1986) but which they claimed to have greater
validity and clinical utility. They concluded that it was a valid and reliable measure of
adherence to psychoactive medications. The patient should be asked to respond to the
statements in the questionnaire by circling the answer which best describes their
behaviour or attitude towards their medication during the past week.
4. Clinician Rating Scale; CRS (Kemp et al, 1996; 1998)
The CRS uses an ordinal scale of 1–7 to quantify the clinician’s assessment of the level
of adherence shown by the patient. Higher numbers represent greater adherence. The
CRS has been used in two controlled trials of ‘compliance therapy’, in which it
demonstrated sensitivity in detecting differences in outcomes among patients receiving
compliance therapy versus non-specific counselling (Kemp et al, 1996; 1998).

5. Medication Adherence Questionnaire (MAQ)


Developer: Morisky-Green, Toll BA, McKee SA, Duong M, Piroth L
The best known and most widely used scales for research adherence is the Medication
Adherence Questionnaire (MAQ) by Morisky et al.4, which has several advantages:
identifies barriers to nonadherence, it is the shortest, easiest to score and very adaptable
for various groups of medication. MAQ identifies barriers to nonadherence but not self-
efficacy.
6. Brief Medication Questionnaire (BMQ)
Developer: Svarstad, Mini, Ben
Brief Medication Questionnaire (BMQ) is a self-report tool for screening adherence and
barriers to adherence. It has three main question headings and multiple sub-questions
9,10. The tool includes:
- 5-item Regimen Screen that asks the patients about their medications that they were
currently taking. Questions are asked to list the name of each medication, frequency of
medication per day, number of days and times they have received each medication along
with the number of times the patient missed taking medications in the past week,
- 2-item Belief Screen consists of two questions that ask the patients whether they had
any difficulty with any of the medications, and does the medication bother them in any
way,
- 2-item Recall Screen assesses the patient’s difficulty in recalling and remembering the
dosage regimen of their medications, and
- 2-item Access screen that evaluates the patient difficulty in buying and refilling their
medications in time
7. The Hill-Bone Compliance Scale
Developer: Kim, Lambert, Koschack, Karademir, Krousel-Wood
The Hill-Bone Compliance Scale addresses barriers and self-efficacy but are limited in
their generalizability. The Hill-Bone Compliance Scale focuses on hypertensive patients.
This scale assesses patient behaviors for three important behavioral domains of high
blood pressure treatment: 1) reduced sodium intake; 2) appointment keeping; and 3)
medication taking. This scale is comprised of 14 items in three subscales. Each item is a
four point Likert type scale (Table 1). The content validity of the scale was assessed by a
relevant literature review and an expert panel, which focused on cultural sensitivity and
appropriateness of the instrument for low literacy.
8. Adherence to Refills and Medications Scale (ARMS)
Developer: Kripalani
The Adherence to Refills and Medications scale (ARMS) is a 12-item scale with high
internal consistency overall (Cronbach’s alpha=0.814) and among patients with
inadequate (alpha=0.792) or marginal/adequate literacy skills (alpha=0.828). Patients
with low ARMS scores (which indicated better adherence) were significantly more likely
to have controlled diastolic blood pressure and tended to have better systolic blood
pressure control. Lexile analysis demonstrated that the instrument had a favorable reading
difficulty level below the eight grades. The ARMS is a valid and reliable medication
adherence scale when used in a chronic disease population, with good performance
characteristics even among low-literacy patients.
9. Self-efficacy for Appropriate Medication Use (SEAMS)
The Self-efficacy for Appropriate Medication Use (SEAMS) was developed by a
multidisciplinary team with expertise in medication adherence and health literacy. Its
psychometric properties were evaluated among 436 patients with coronary heart disease
and other comorbid conditions7. Reliability was evaluated by measuring internal
consistency and test-retest reliability. The final 13-item scale had good internal
consistency reliability (Cronbach’s alpha=0.89). The SEAMS is a reliable and valid
instrument that may provide a valuable assessment of medication self-efficacy in chronic
disease management, and appears appropriate for use in patients with low literacy skills.
10. Adherence Scale Culig

SCALES SUITABLE FOR MEASURING ADHERENCE AT CERTAIN DISEASES


ACTIVITY NO 18
TO DEVELOP A PHARMACEUTICAL CARE PLAN FOR DIABETES MELLITUS
PATIENTS

PATIENT CARE PROCESS


1. Collect information:
 Perform medication history of prescription, over-the-counter, and herbal product use.
 Collect laboratory data including chemistry panel, A1c, lipid panel, and albumin-to-
creatinine ratio.
 Measure BP.
 Examine patient for development or progression of DM complications.
 Record SMBG, including FPG and postprandial levels.
 Interview patient to gather information related to quality of-life measures such as
physical, psychological, and social functioning and well-being.
2. Assess the information:
 SMBG for glycaemic control, including FPG and postprandial levels (See table 1).
 Are the BG values too high or low?
 Are there specific times of day or specific days not within glucose goals?
 Is hypoglycemia occurring?
 Review laboratory data for attainment of goals. What goals are not being met?
 Are there any medication problems, including presence of adverse drug reactions, drug
allergies, and drug interactions?
 Is the patient taking medications that may affect glucose control?
 If patient is already receiving treatment for DM, has he/she been adherent to
recommended lifestyle modifications and drug therapies? Is the patient having difficulty
affording their therapies?
 Assess patient for quality-of-life measures such as physical, psychological, and social
functioning and well-being.
3. Develop a care plan:
 Recommend appropriate therapy and develop a plan to assess.(refer to the previous
activity to view treatment options & fig A, B, C)
4. Implement the care plan
 Stress adherence to prescribed lifestyle and medication regimen.
 Ensure patient has prescription coverage and/or is able to afford prescribed regimen and
self-care.
 Provide education on diabetes, lifestyle modifications, appropriate monitoring, and drug
therapy.
 Causes of DM complications and how to prevent them.
 How diet and exercise can affect diabetes.
 How to perform SMBG and what to do with the results.
 When to take medications and what to expect, including adverse effects.
 What warning sign(s) should be reported to the provider?
 What tests or referrals to other health care team members are needed?
FIGURE A
5. Follow-up: monitor and evaluate

 Set follow-up for SMBG and tolerability/presence of adverse effects based on therapy
chosen.
 Follow-up A1c every 3 months until patient reaches goal, then every 6 months (see table
43-6 for monitoring parameters and frequency)
 Monitor for macrovascular and microvascular signs and symptoms. (TABLE A)

MACROVASCULAR AND MICROVASCULAR COMPLICATIONS SIGNS AND SYMPTOMS


COMPLICATIONS SIGNS & SYMPTOMS
Macrovascular Coronary Heart Stable or unstable angina pectoris, MI, or dysrhythmias;
disease however, many patients have unrecognizable symptoms.
PAD Exertional leg pain that can progress to pain at rest and
ischemic ulcers. Most cases are asymptomatic
CerebroVascular/disease Sudden onset of a focal neurologic deficit such as facial
or stroke droop, hemiparesis, or isolated weakness of an arm or leg.
Dizziness, slurred speech, gait difficulties, and visual loss
may also occur.
Microvascular Retinopathy Minimal until advanced disease ensues with loss or blurring
of vision.
Nephropathy Hypertension, which often coincides with the development of
microalbuminuria (persistent proteinuria)

Neuropathy Numbness, tingling, burning, muscle pain/ cramps/weakness


that often gets worse at night
Foot Care (Neuropathy Calluses and corns, tinea pedis, hammertoes, bunions,
and/ or PAD) cracking of skin of the feed and heels.

AMERICAN DIABETES ASSOCIATION RECOMMENDED GOALS OF THERAPY IN ADULTS.


AREA GOALS
Glycemia A1c < 7% (0.07; 53 mmol/mol Hgb) Evaluate every 3 months until in
goal; then every 6 months
Preprandial plasma glucose 80–130 mg/dL (4.4–7.2 mmol/L)
Peak postprandial plasma glucosea < 180 mg/dL (10.0 mmol/L)
Blood pressure < 140/90 mm Hg Evaluate at every visit
Lipids Evaluate at diagnosis and/or age 40, then every 1–2 years thereafter
Monitoring for complications Dilated eye examination yearly Feet should be examined at every
Eyes visit Urinary microalbumin Yearly
Feet
Urinary micro albumin
TABLE 1

Activity # 19:
Design for pharmaceutical plan for the tuberculosis patients

 Patient Care Process:


 Collect Information:
 Obtain a thorough medical and medication history.
 Obtain necessary laboratory tests, cultures, and radiology to determine active
infection. (Collect appropriate samples for smears and cultures.)
 Review physical assessment findings.
 Speak with the patient obtain risk factors for infection and risk factors for developing
active TB (travel, living conditions, immune status, etc).
 Assess the Information:
 Assess the patient’s risk factors and signs and symptoms to determine whether the
patient might be infected with TB.
 Based on physical examination, medical history, laboratory tests and cultures, and X-
rays, determine whether the patient has an active TB infection.
 Assess the efficacy, safety, and patient adherence of required pharmacotherapy.
 Identify any significant adverse drug effects or interactions
 Develop a Care Plan:
 Isolate the patient with active disease to prevent the spread of the disease.
 Select and recommend appropriate anti-tuberculosis treatment. Consider
susceptibility, HIV status, drug interactions, type of TB infection, etc.
 Choose medication doses that are optimal for the patient. Consider renal function,
liver function, etc.
 Consider DOT.
 Identify the index case that infected the patient, identify all persons infected by both
the index case and the new case of TB, and the complete appropriate treatments for
those individuals.
 Implement the Care Plan:
 Review drugs, duration, dose, frequency, and side effects of selected medications.
 Educate the patient about the importance of compliance with the regimen and the
risks of noncompliance.
 Ensure adherence to the treatment regimen by the patient.
 Follow-up: Monitor and Evaluate:
 Follow-up at required intervals to obtain AFB stains to evaluate the effectiveness of
treatment.
 Review susceptibilities when available and modify treatment regimen as determined
by susceptibility results.
 Continue treatment for at least 6 months from the time that the patient converts to a
negative culture.
 Consider TDM if no clinical improvement.

 General Approaches to Treatment:


The primary treatment approach is the use of antimicrobials active against M. tuberculosis. Once active
disease is present, typically three or four drugs must be used simultaneously from the outset of treatment.
The shortest duration of treatment is 4 months in the unusual case of smear and culture negative clinical
cases of pulmonary TB, and up to 2 years of treatment may be necessary for advanced cases of MDR-TB.
Directly observed treatment (DOT) is a method used to ensure adherence in which patients are directly
observed by a health care worker while taking their anti-tuberculosis medication.

 Pharmacologic therapy:
ACTIVITY NO 20

Supportive Care for Cancer Patients


Supportive Care.

Patients with cancer are at risk for serious adverse events that results from their treatment, the
cancer, or both. The management of these complications is generally referred to as supportive
care (or symptom management).

CHEMOTHERAPY-INDUCED TOXICITIES

NAUSEA/VOMITING

Nausea and vomiting are among the most commonly feared toxicities by patients undergoing
chemotherapy.1 The optimal method of managing CINV is to provide adequate pharmacologic
prophylaxis given a patient’s risk level for emesis. Insufficient control during the first cycle of
chemotherapy leads to more difficulty in controlling emesis for subsequent cycles.

Treatment-related complications.

1. Chemotherapy-induce nausea and vomiting ( CINV)

CINV is one of the adverse effects of chemotherapy nausea and vomiting are among the most
commonly feared toxicities by patients undergoing chemotherapy.

 Clinical presentation and Diagnosis of CINV

Acute Nausea/vomiting

 Occurs within the first 24 hours after chemotherapy administration

Delayed Nausea/Vomiting

 Occurs between 24 hours and 5 days after chemotherapy administration

Anticipatory Nausea/Vomiting

 A learned, conditioned reflex response to a stimulus (sight, sound, smell) often associated
with poor emetic control in a pervious cycle of chemotherapy
Breakthrough Nausea/Vomiting

 Occur despite prophylaxis with an appropriate antiemetic regimen

Differential Diagnosis

 Surgery, radiation, Brain metastases, Gastric outlet or bowel obstruction, constipation.


Hypercalcemia, hyperglycemia, hyponatremia, uremia, Food poisoning or intolerance
 Other drugs(opioids)

Treatment

General approach to treatment CINV

Agents Agents
High emetic risk Low emetic risk
AC combination (doxorubicin or epirubicin and Ado-trastuzumab emtansine, Afatinub( oral),
cyclophosphamide) Amifostine,Bexarotene, Brentuximab,
Carmustine ,Carboplatin, crizotinib Cabazitaxel, Carfilzomib, Capecitabine, Dasatinib
cyclophosphamide, Dacarbazine, doxorubicin , Docetaxel, Doxorubicin, Eribulin, Erlotinib,
Epirubicin ,etoposide ,ifosfamide, temozolomide Etoposide, Gemcitabine, Ixabepilone, 5-
Moderate emetic risk Fluorouracil, Methotrexate, Mitomycin,
Amifostine ,Arsenic trioxide, Azacitidine, Mitoxantrone, Paclitaxel, Paclitaxel, palbociclib,
Bendamustine, Busulfan, carboplatin pametrexed, sunitinib(oral), topotecan, vorinostat
Carmustine,cyclosposphamide, cytarabine
Daunorubicin, Epirubicin, Idarubicin, Isosfamide,
Irintecan, Methrexate, Oxliplatin

Nonpharmacologic Therapy Pharmacologic Therapy


1. Behavior therapies such as relaxation,  Nonprescription medications such as
guided imagery, and music therapy and antacids, histamine-2 receptor blocker
acupuncture or acupressure blockers, and proton pump inhibitors.
2. Other general measures that can be taken  Corticosteroids (dexamethasone),
include ensuring adequate sleep before serotonin receptor antagonists, NKI
treatment, eating small meals, and receptor antagonist (aprepitant or
avoiding spicy and greasy foods and foods fosaprepitant), and the
with strong odors. thienobenzodiazepine regimen.

2. Mucositis

Mucositis is the inflammation of the mucosal lining in the oral cavity and Gi tract caused by
damage from radiation or cytotoxic chemotherapy, often leading to ulcers.

Clinical Presentation and Diagnosis of Mucositis

 Painful, erythematous ulcers develop on the lips, cheeks, soft palate, floor of mouth, and
throughout the entire gastrointestinal tract
 Assess mucositis using validated scales, either oral mucositis assessment scale (OMAS)
or Patient-Reported Oral Mucositis Symptom (PROMS) Scale
 Symptoms appear within 5 to 7days after chemotherapy and resolve in 2 to 3 weeks.
 Pain may affect ability to swallow and eat.
 The patient may have concomitant localized or systemic infection.
 Diarrhea is a symptom of mucositis in the lower GI tract, can lead to electrolyte
imbalances.

Treatment

Nonpharmacologic Treatment Pharmacologic Treatment


 Good oral hygiene (brushing with a  Amifostine , Intrarectal before each dose of
soft- bristled toothbrush at least twice radiation therapy for rectal cancer to prevent
daily, flossing, bland rinses, and saliva GI mucositis.
substitutes) and maintaing optimal  Gelclair, Caphasol, and Biotene gels.
nutritional support.  Benzydamine mouthwash.
 Cryotherapy with ice chips is also  Ranitidine or omeprazole orally recommended
helpful for patients at risk for to prevent pain associated with mucositis and
mucositis who are receiving 5- FU- reflux following offending chemotherapy.
based chemotherapy.  Octreotide at a dose of at least 100 mcg
 Low- level laser therapy is also useful subcutaneously twice daily is recommended to
to prevent mucositis in the treat mucositis- related diarrhea associated
hematopoietic cell transplant (HCT) with high- dose stem cell transplantation if
setting. loperamide is ineffective.
 Pain management may be achieved with oral
or intravenous opioids, topical anesthetic
products, and compounded rinses that
incorporate lidocaine.
 Antimicrobial therapy is necessary to prevent
systemic infection.
 Palifermin IV bolus injection for the
prevention and treatment of mucositis.

3. Hematologic complications; Febrile Neutropenia (FN)

FN is a common adverse effect after administration of cytotoxic chemotherapy. Patients


frequently require hospitalization for prompt administration of broad- spectrum antibiotics that
are critical to avoid morbidity and mortality.

Clinical Presentation and Diagnosis of FN

Signs and symptoms

 Fever is the only sign of infection, although septic patients may have chills.
 Infected catheter sites may be erythematous and tender to the touch.

Laboratory Tests

 CBC with differential


 Two blood cultures from each access site (peripheral and central), urinalysis, urine
culture, chest x-ray, sputum cultures.

Other Diagnostic Tests


 Detailed physical examination of the oral mucosa, sinuses, skin, catheter access sites,
perineal area (no rectal examination because of the risk of bacteremia)

Treatment

Non- pharmacologic Therapy Pharmacologic Therapy


 Handwashing, Influenza vaccines, Monotherapy
 Cefepime
pneumonia and meningococcal vaccine.
 Ceftazidime or
 Wound debridement should perform  Carbapenem
upon catheter removal Dual Therapy
Aminoglycosides and
 Use of high efficiency particulate air
 Antipseudomonal penicillin,
(HEPA) filtration systems in patients'  Cefepime
rooms.  Ceftazidime or
 Vancomycin needed
 Cefepime
 Ceftazidime, or
 Carbapenem with or without
aminoglycosides.

4. Cardiovascular complications; Superior vena cava syndrome (SVCS)

Superior vena cava syndrome is a relatively rare complication that may occur in patients with
cancer. SVCS is rarely immediately life threatening except in patients with airway compromise
and/or laryngeal or cerebral edema. However, rapid recognition of typical presenting symptoms
facilitates referral for tissue diagnosis (if unknown) and treatment.

Clinical presentation and diagnosis of SVCS

Signs and symptoms

 Most common; swelling of face, neck, and upper extremity edema, dyspnea, cough,
dilated upper extremity veins.
 Less common; hoarseness, dysphagia, dizziness, headache, lethargy, chest pain.
 Patients with elevated ICF may have mental status changes.
 Patients with airway obstruction may have shortness of breath.
Diagnostic tests

 Tissue biopsy to determine underlying malignancy (if unknown), chest x-ray, Ct scan,
bronchoscopy, mediastinoscopy.

Treatment

Non-pharmacologic Therapy Pharmacologic Therapy


1. Radiation therapy is the treatment of choice 1. Cytotoxic chemotherapy for chemotherapy –
for chemotherapy- resistant tumors such as sensitive tumors such as SCLC, and lymphoma.
non- small cell lung cancer (NSCLC) OR in 2. Corticosteroids in the management of SVCS, and
chemotherapy- refractory patients with SVCS. lymphoma.
2. Radiation therapy is also be combined with 3. Diuretics (furosemide) used with diligent
chemotherapy for chemotherapy –sensitive monitoring of the patient's fluid status and blood
tumors such as SCLC and lymphoma. pressure.
3. Surgical options for the management of 4. Thrombosis-related SVCS, anticoagulation with
SVCS include stent placement and surgical heparin and warfarin, thrombolytic (alteplase) in
bypass, SVCS stenting may provide longer- patients with thrombosis caused by indwelling
term relief of symptom. catheters.

5. Neurologic complications; spinal cord compression

Spinal cord compression is an oncologic emergency because delays in treatment by mere hours
may lead to permanent neurologic dysfunction.

Clinical presentation and diagnosis of spinal cord compression

 Once neurologic deficits appear, progression to irreversible paralysis may occur with
hours to days.

Signs and symptoms

 Back pain, aggravated by movement, supine positioning, coughing, sneezing, neck


flexion, straight leg raises, Valsalva maneuver, palpation of spine, sensory deficit.
 Cervical spine compression(quadriplegia), thoracic spine compression (paraplegia), upper
lumbar spine compression (bowel and bladder dysfunction (constipation and urinary
retention) and abnormal extensor plantar reflexes, weakness.

Diagnostic Tests

 MRI with gadolinium enhancement is the gold standard


 x-rays may be helpful to identify to identify bone abnormalities

Treatment

Non- pharmacologic therapy Pharmacologic therapy


 Radiation therapy  Corticosteroids
 Laminectomy  Dexamethasone to reduce edema, inhibit
inflammation, and delay the onset of
neurologic complications.
 Opioid analgesics used and titrated rapidly
to achieve adequate pain control

5. Brain Metastases

Brain metastases are the most feared complications of cancer and generally carry a poor
prognosis. Serious consequence of brain metastases is elevated ICP, which can rapidly lead to
fatal intracranial herniation and death.

Clinical presentation and diagnosis of brain metastasis

General

 Almost all patients with brain metastases are symptomatic.


 New cerebral neurologic symptoms in a cancer patient should initiate evaluation for brain
metastases.
 Other causes of brain lesions, including hemorrhage, infection, and infarct, should be
ruled out.

Signs and symptoms

 Mental status changes (loss of consciousness, irritability, confusion)


 Hemiparesis, aphasia, papilledema, weakness, seizure, nausea, vomiting and headache.
Treatment

Non-pharmacologic therapy Pharmacologic therapy


 Radiation therapy (whole- brain  Corticosteroids reduce edema.
radiation).  Mannitol used in patients with
 Stereotactic radiosurgery using a impending cerebral herniation.
linear accelerator or gamma knife.  Phenytoin 15mg/kg, diazepam 5mg IV
 Prophylactic cranial irradiation (PCI). used for rapid control of persistent
 Surgery seizures.

6. Hemorrhagic cystitis

Hemorrhagic cystitis is defined as acute or insidious bleeding from the lining of the bladder.

Clinical presentation and diagnosis of hemorrhagic cystitis.

Signs and symptoms

 Suprapubic pain, cramping, urinary urgency and frequency, dysuria, burning and
hematuria
 Urinary retention leading to hydronephrosis and renal failure may.

Laboratory Tests

 Urine dipsticks for blood, microscopic hematuria, CBC, Prothrombin time, international
normalized ratio, activated partial thromboplastin time, BUN, creatinine.

Treatment

Non-Pharmacologic therapy Pharmacologic therapy


 Facilitate saline lavage and evacuation  Local agents, systemic agents and hemostatic
of blood clots. agents such as alum, prostaglandins, silver
 Surgical removal of blood clots. nitrate, and formalin
 Urinary diversion with percutaneous  Systemic agents including estrogens,
nephrotomy or surgical removal of vasopressin, aminocaproic acid, and hyperbaric
bladder. oxygen (HBO)
 Antispasmodic agents such as oxybutynin 5mg,
opioid analgesics titrated to adequate pain.
 Surgical procedures may be warranted.

7. Hypercalcemia of Malignancy

Hypercalcemia is the metabolic abnormality experienced by patients with cancer.it is associated


with poor prognosis because of the frequent association with advanced or metastatic disease.

Clinical presentation and diagnosis of hypercalcemia.

Signs and symptoms

 Lack of appetite, nausea, vomiting, constipation, weakness, bone pain, fatigue, ataxia,
confusion, headache, lethargy, seizures, coma, polydipsia, polyuria, renal failure,
bradycardia abnormalities, arrhythmias.

Laboratory Tests

 Elevated corrected serum calcium level, low serum albumin, low to normal serum
phosphate.
 BUN, serum creatinine, elevated alkaline phosphate and ECG.

Other diagnostic tests

 Primary hyperparathyroidism, hyperthyroidism, vitamin D intoxication, chronic renal


failure.

Treatment

Non-pharmacologic therapy Pharmacologic therapy


 Calciuric therapy in the form of  Calciuric therapy (IV normal saline and
hydration used to treat hypercalcemia. furosemide)
 Dialysis used in patients who cannot  Antiresorptive therapy (Pamidronate,
tolerate aggressive saline hydration. zoledronic acid, corticosteroids, calcitonin,
gallium nitrate, Denosumab)
8. TLS (Tumor lysis syndrome)

TLS is the result of rapid destruction of malignant cells with subsequent release of intracellular
contents into the circulation. It may cause morbidity and mortality.

Clinical presentation and diagnosis of TLS

Signs and symptoms

 Asymptomatic, edema, fluid overload, oliguria, hyperuricemia, nausea, vomiting,


lethargy, hyperkalemia, muscle weakness, paresthesia, ECG changes, bradycardia,
hypocalcemia, muscle cramps, tetany, irritability, paresthesias, arrhythmias.

Laboratory Tests.

 Serum uric acid, serum potassium, serum phosphorus, serum calcium, elevated BUN,
creatinine.

Treatment

Non- pharmacologic therapy Pharmacologic therapy


 IV hydration (DW5 with normal  Oral allopurinol (Zyloprim)
saline).  N allopurinol ( Aloprim)
 Hemodialysis.  Rasburicase ( Elitek)
ACTIVITY NO 21
INTRODUCTION TO PHARMACOECONOMIC ANALYSIS WITH PRACTICE
EXAMPLES.

1. PHARMACOECONOMICS:-
The process of identifying, measuring, and comparing the costs, risks, and benefits of programs,
services, or therapies and determining which alternative produces the best health outcome for
the resource invested.
2. COST:-
It is defines as the value of resource consumed by a program or drug therapy of interest
3. CONSEQUENCE:-
It is defined as the effects, outputs, or outcomes of the program of drug therapy of interest.
4. COST OF ILLNESS EVALUATION (COI):-
It identifies and estimates the overall cost of a particular disease for a defined population. It
involves measuring the direct and indirect costs attributable to a specific disease. The cost of
diseases such as mental disorders, and cancer can be estimated.
5. COST MINIMIZATION ANALYSIS (CMA):-
It involves the determination of the least costly alternative when comparing two or more
treatment alternatives. In this costs can be measured in competing monetary units (euros).
6. COST BENEFIT ANALYSIS (CBA):-
It is the method that allows for the identification of measurement, and comparison of the
benefits and costs of a program or treatment alternative.
7. COST EFFECTIVE ANALYSIS (CEA):-
It involves comparing programs or treatment alternatives with different safety and efficacy
profiles.
Cot to effective ratio = COSTS / therapeutic effect in measurable units
8. COST UTILITY ANALYSIS (CUA):-
It is a method for comparing treatment alternative that integrates patient preferences. It can
compare costs, quality, and the quantity of patient-years. Often the utility measurement used is
quality-adjusted life year (QALY) gained.

9. DISABILITY ADJUSTED LIFE YEARS (DALYs):-


DALYs for a disease are the sum of the years of life lost due to premature mortality in the
population and the year lost due to disability cases of the incident cases of health year.

NUMERICAL PROBLEMS
QUESTION NO 1:
A hospitalized patient was switched from IV ciprofloxacin 400mg given every 2h to oral
ciprofloxacin 500mg every 12. Calculate daily cost if IV product is 120 PKR per 200mg and
Oral product is 29.5 PKR per 250mg?
QUESTION NO 2:-
Verapamil Immediate release (IR) 80 mg tablets are taken 3 times a day & its cost is 7.52Rs per
100 tablets. Extended release (ER) capsules of Verapamil are 240mg once daily and cost is
15.52 Rs per 100 capsules. Calculate treatment cost differential over 30 days period.
QUESTION NO 3:-
Hypothetical medicines A & B have been compared by randomized trials in which the primary
outcome of mortality was measured 30 days after the randomization. Outcome of 100 patients is
given as
 No treatment = 15 deaths
 Treatment A = 10 deaths
 Treatment B = 7 deaths
 Drug A = 200 Rs
 Drug B = 1000Rs
QUESTION NO 4:-
What is incremental cost per life saved for each day compared to no treatment? What is ICE
ratios and express them as equivalent cosr pr life gained. Assume 8y of survival per life gained.

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