Professional Documents
Culture Documents
(CLINICAL PHARMACY-II)
Practical Activities
Notebook
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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.
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.
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.
• Overweight: BMI is 25 to 29.9kg/m2
• 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)
TYPES OF GLUCOMETER:-
1. Standard
2. Continuous.
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.
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.
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.
PROCEDURE:-
A. METHOD TO CALCULATE BMI:
• 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.
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).
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
OBSERVATIONS:-
PRECAUTIONS:-
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:-
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.
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.
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.
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),
3. Prioritize the health-care facility core elements based on the situational analysis:
5. Develop a health-care facility AMS action plan that specifies the human and financial resources
required.
8. Offer basic and continued educational resources and training on optimized antibiotic prescribing.
7. Up-to-date clinical guidelines that include AMS principles and integrate the AWaRe classification of
□ □
antibiotics
18. National surveillance system on AMR in place with laboratory capacity to guide optimal use
AND DATA
Yes No
HEALTH-CARE FACILITY CORE ELEMENTS
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
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
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
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
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
1. Overprescribing Antibiotics are prescribed when not needed, e.g. fever without evidence of infection,
Inflammatory conditions.
2. Overly broad More broad-spectrum antibiotics (WATCH and RESERVE antibiotics) are prescribed than
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
9. Delayed administration Administration of the antibiotic(s) is delayed from the time of prescription. Repeat doses
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
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
Approver
Fosfomycin (intravenous)
Linezolid -Multi-drug resistant
Mycobacterium
tuberculosis
-Vancomycin resistant
Enterococcus
-Vancomycin resistant
Staphylococcus aureus
-Methicillin resistant
Staphylococcus aureus
ACTIVITY NO 6
INTRODUCTION TO DIFFERENT (EML) AND COMPARISON
BETWEEN WHO AND PAKISTAN’S ESSENTIAL MEDICINE LIST’S.
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.
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.
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.
(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.
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
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
Diagnosis
Age/Sex/Weight
Date Treated
CRITERIA AND INDICATORS Threshold Observed
Diagnosis
Age/Sex/Weight
Date Treated
Outcome Indicators:
8. Clinical improvement noted in patient medical 100% YES NO YES NO YES NO YES NO
records
Diagnosis
Age/Sex/Weight
Date Treated
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)
Diagnosis
Age/Sex/Weight
Date Treated
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%
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 =?
( 140−72 ) ×83
=
2.5 × 72
=31ml/min.
298(31)
= 226 +
29.1+ 31
= 380L
D
Maintenance Dose = =C ss Cl / F where F = 0.7
τ
= 1.5 × 380
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 =?
= 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
2 ko 2Vd (C 1+C 2 )
CL = +
C1 +C 2 ( C1 +C 2 ) (t 2 −t 1 )
=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 =?
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
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
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
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
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:
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.
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.
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)
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.
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.
180mg/dL 2 units
220 3 units
260 4 units
300 5 units
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.
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.
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:
• 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.
3. Patient instructed to monitor blood glucose AC and HS and bring information on RTC.
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.
QUESTIONS:
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:
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?
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?
1. The most common rodenticides available today are the “superwarfarins,” brodifacoum,
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
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
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
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.
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
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
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)
Activity # 19:
Design for pharmaceutical plan for the tuberculosis patients
Pharmacologic therapy:
ACTIVITY NO 20
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.
CINV is one of the adverse effects of chemotherapy nausea and vomiting are among the most
commonly feared toxicities by patients undergoing chemotherapy.
Acute Nausea/vomiting
Delayed Nausea/Vomiting
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
Differential Diagnosis
Treatment
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
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.
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
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
Treatment
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.
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
Spinal cord compression is an oncologic emergency because delays in treatment by mere hours
may lead to permanent neurologic dysfunction.
Once neurologic deficits appear, progression to irreversible paralysis may occur with
hours to days.
Diagnostic Tests
Treatment
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.
General
6. Hemorrhagic cystitis
Hemorrhagic cystitis is defined as acute or insidious bleeding from the lining of the bladder.
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
7. Hypercalcemia of Malignancy
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.
Treatment
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.
Laboratory Tests.
Serum uric acid, serum potassium, serum phosphorus, serum calcium, elevated BUN,
creatinine.
Treatment
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.
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.