This document discusses drug interactions, defining them as when the effect of one drug is modified by another drug taken at the same time. It notes several key risk factors for interactions like polypharmacy and lists common outcomes like increased or decreased therapeutic effects and toxicity. The main mechanisms of interactions are pharmacokinetic, involving absorption, distribution, metabolism and excretion, or pharmacodynamic involving the drugs' pharmacological effects. Several examples of interaction mechanisms are provided like enzyme induction/inhibition altering metabolism or drug complexes reducing absorption. Managing interactions may require dose changes or avoiding certain combinations depending on severity.
A drug interaction is a situation in which a substance affects the activity of a drug, i.e. the effects are increased or decreased, or they produce a new effect that neither produces on its own.
A drug interaction is a situation in which a substance affects the activity of a drug, i.e. the effects are increased or decreased, or they produce a new effect that neither produces on its own.
Drug interaction is defined as the pharmacological activity of one drug is altered by the concomitant use of another drug or by the presence of some other substance
The Drug whose Activity is effected by such an Interaction is called as a “Object drug.”
The agent which precipitates such an interaction is referred as the “Precipitant”.
Drug interaction is defined as the pharmacological activity of one drug is altered by the concomitant use of another drug or by the presence of some other substance.
1.Drug-drug interactions.
2.Drug-food interactions.
3.Chemical-drug interactions.
4.Drug-laboratory test interactions.
5.Drug-disease interactions.
DRUG INTERACTIONS (MECHANISMS OF DRUG-DRUG INTERACTIONS)N Anusha
A Drug interaction is an interaction between a drug and some other substance, such as another drug or a certain type of food, which leads to interaction that could manifest as an increase or decrease in the effectiveness or an adverse reaction or a totally new side effect that is not seen with either drug alone that can be severe enough to alter the clinical outcome.
Every time a drug is administered with any other prescription medicine, OTC products, herbs or even food we expose ourselves to the risk of a potentially dangerous interaction.
this ppt deals with different types of drug interactions with examples and highlights important principles in monitoring drug therapy....for better understanding of complexity of multiple drug usage (polypharmacy)
Al Azhar University | Faculty of Pharmacy | Class of 2018 Graduation Project (Drug Interactions).
in both parameters Drug Drug Interactions and Drug Food Interactions.
A drug interaction is a situation in which a substance (usually another drug) affects the activity of a drug when both are administered together.
Drug interaction is defined as the pharmacological activity of one drug is altered by the concomitant use of another drug or by the presence of some other substance
The Drug whose Activity is effected by such an Interaction is called as a “Object drug.”
The agent which precipitates such an interaction is referred as the “Precipitant”.
Drug interaction is defined as the pharmacological activity of one drug is altered by the concomitant use of another drug or by the presence of some other substance.
1.Drug-drug interactions.
2.Drug-food interactions.
3.Chemical-drug interactions.
4.Drug-laboratory test interactions.
5.Drug-disease interactions.
DRUG INTERACTIONS (MECHANISMS OF DRUG-DRUG INTERACTIONS)N Anusha
A Drug interaction is an interaction between a drug and some other substance, such as another drug or a certain type of food, which leads to interaction that could manifest as an increase or decrease in the effectiveness or an adverse reaction or a totally new side effect that is not seen with either drug alone that can be severe enough to alter the clinical outcome.
Every time a drug is administered with any other prescription medicine, OTC products, herbs or even food we expose ourselves to the risk of a potentially dangerous interaction.
this ppt deals with different types of drug interactions with examples and highlights important principles in monitoring drug therapy....for better understanding of complexity of multiple drug usage (polypharmacy)
Al Azhar University | Faculty of Pharmacy | Class of 2018 Graduation Project (Drug Interactions).
in both parameters Drug Drug Interactions and Drug Food Interactions.
A drug interaction is a situation in which a substance (usually another drug) affects the activity of a drug when both are administered together.
Pharmacokinetic interactions of Smoking with drugs such as Duloxetine (SNRI Antidepressant), Fluvoxamine (SSRI Antidepressant), Tricyclic Antidepressants ( Amitriptyline, Clomipramine, Imipramine, Nortriptyline, etc.), Benzodiazepines (Alprazolam, Chlordiazepoxide, Clonazepam, Diazepam, Loprazolam, Lorazepam, Lormetazepam, Nitrazepam, Oxazepam, Temazepam), Antipsychotics (Olanzapine, Clozapine, Haloperidol, Thioridazine, Chlorpromazine and Fluphenazine), Opioids (Methadone, Dextropropoxyphene, Fentanyl, Hydrocodone, Oxycodone, Morphine, Nalbuphine and Pethidine (Meperidine)), NSAIDs (Diflunisal, Phenazone and Phenylbutazone), Paracetamol (Acetaminophen), Theophylline, Caffeine, Tacrine, Insulin and Warfarin are discussed in this presentation.
Pharmacodynamic interactions of Smoking with drugs like Beta blockers, Benzodiazepines, Oral antidiabetics, Inhaled corticosteroids and Oral contraceptive pills are also dealt in this presentation.
A powerful presentation on the good and bad sides of drug interactions with examples. It may be used for academic purpose only. These days because of polypharmacy it has become necessary for all of us to be aware of possible drug interactions and how to avaoid them in order not to cause other detrimental conditions. All the major types of drug interactions are discussed here. It should be noted that reading other materials on drug interactions will also enhance your understanding of this intricate process.
Drug interactionPharmacokinetic and Pharmacodynamic drug interaction| Drug-fo...Shaikh Abusufyan
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These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
2. Defination
• It is the modification of the effect of one drug (the object
drug ) by the prior concomitant administration of
another (precipitant drug).
• Concomitant use of several drug in presence of another
drug is often necessory for achiving a set of goal or in the
case when the patient is suffering from more than one
disease.
• In these cases chance of drug interction coud increase.
3. • Defination
• Epidemiology
• Risk factor
• Out come of interaction
• Mechanism of interaction
a.pharmacokinetic
b.pharmacodynemic
• Case study
• Reference
4. • In harvard medical practice study of adverse event 8%
were consider to be due to drug interaction.
• US community pharmacy study revealed 4.1 %
incidence of drug interaction in hospitalised patient.
• Australian study found that 4.4% of all ADR , which
resulted in hospital due to interaction.
5. • Poly pharmacy
• Multiple prescribers
• Multiple pharmacies
• Genetic make up
• Specific population like e.g,
females , elderly, obese, malnouresed , criticaly ill
patient , trasplant recipient
• Specific illness E.g. Hepatic disease,
Renal dysfunction,
• Narrow therapeutic index drugs
Cyclosporine, Digoxin, Insulin, Lithium ,
Antidepressant, Warfarin
6. Outcomes of drug interactions
1) Loss of therapeutic effect
2) Toxicity
3) Unexpected increase in pharmacological activity
4) Beneficial effects e.g additive & potentiation (intended)
or antagonism (unintended).
5) Chemical or physical interaction
e.g I.V incompatibility in fluid or syringes
mixture
7. Mechanisms of drug interactions
Pharmacokinetics Pharmacodynamics
Pharmacokinetics involve the effect of a drug on another drug
kinetic that includes absorption ,distribution , metabolism
and excretion.
Pharmacodynamics are related to the pharmacological
activity of the interacting drugs
E.g., synergism , antagonism, altered cellular transport effect
on the receptor site.
8. Pharmacokinetic interactions
1) Altered GIT absorption.
•Altered pH
•Altered bacterial flora
• formation of drug chelates or complexes
• drug induced mucosal damage
• altered GIT motility.
a) Altered pH;
The non-ionized form of a drug is more lipid
soluble and more readily absorbed from GIT than the
ionized form does.
9. Ex1., antiacids Decrease the tablet
dissolution
of Ketoconazole (acidic)
Ex2., H2 antagonists
Therefore, these drugs must be separated by at least 2h
in the time of administration of both .
10. b) Altered intestinal bacterial flora ;
EX., 40% or more of the administered digoxin dose is
metabolised by the intestinal flora.
Antibiotics kill a large number of the normal
flora of the intestine
Increase digoxin conc.
and increase its toxicity
11. c) Complexation or chelation;
EX1., Tetracycline interacts with iron preparations
or
Milk (Ca2+ ) Unabsorpable complex
Ex2., Antacid (aluminum or magnesium) hydroxide
Decrease absorption of
ciprofloxacin by 85%
due to chelation
12. d) Drug-induced mucosal damage.
Antineoplastic agents e.g., cyclophosphamide
vincristine
procarbazine
Inhibit absorption
of several drugs
eg., digoxin
e) Altered motility
Metoclopramide (antiemitic)
Increase absorption of cyclosporine due
to the increase of stomach empting time
Increase the toxicity
of cyclosporine
13. f) Displaced protein binding
It depends on the affinity of the drug to plasma protein.
The most likely bound drugs is capable to displace others.
The free drug is increased by displacement by another drug
with higher affinity.
Phenytoin is a highly bound to plasma protein (90%),
Tolbutamide (96%), and warfarin (99%)
Drugs that displace these agents are Aspirin
Sulfonamides
phenylbutazone
14. g) Altered metabolism
The effect of one drug on the metabolism of the
other is well documented. The liver is the major site of drug
metabolism but other organs can also do e.g., WBC,skin,lung,
and GIT.
CYP450 family is the major metabolizing enzyme
in phase I (oxidation process).
Therefore, the effect of drugs on the rate of metabolism
of others can involve the following examples.
15. E.g., Enzyme induction
A drug may induce the enzyme that is responsible
for the metabolism of another drug or even itself e.g.,
Carbamazepine (antiepileptic drug ) increases its own
Metabolism.
Phenytoin increases hepatic metabolism of theophylline
Leading to decrease its level Reduces its action
and
Vice versa
N.B enzyme induction involves protein synthesis .Therefore,
it needs time up to 3 weeks to reach a maximal effect
16. Eg., Enzyme inhibition;
It is the decrease of the rate of metabolism of a drug by
another one .
This will lead to the increase of the concentration of the
target drug and leading to the increase of its toxicity .
Inhibition of the enzyme may be due to the competition
on its binding sites , so the onset of action is short
may be within 24h.
When an enzyme inducer ( e.g. carbamazepine) is
administered with an inhibitor (verapamil)
The effect of the
inhibitor will be
predominant
17. Ex.,Erythromycin inhibit metabolism of astemazole and terfenadine
Increase the serum conc.
of the antihistaminic leading to
increasing the life threatening
cardiotoxicity
EX., Omeprazole
Inhibits oxidative
metabolism
of diazepam
18. •Onset of drug interaction
It may be seconds up to weeks for example in case
of enzyme induction, it needs weeks for protein synthesis,
while enzyme inhibition occurs rapidly.
The onset of action of a drug may be affected by the half
lives of the drugs
e.g., cimitidine inhibits metabolism of theophylline.
Cimitidine has a long half life, while, theophylline has a short
one.
When cimitidine is administered to a patient regimen for
Theophylline, interaction takes place in one day.
19. First-pass metabolism:
Oral administration increases the chance for liver
and GIT metabolism of drugs leading to the loss of a
part of the drug dose decreasing its action. This is
more clear when such drug is an enzyme inducer
or inhibitor.
EX., Rifampin lowers serum con. of verapamil level by
increase its first pass . Also, Rifampin induces the
hepatic metabolism of verapamil
20. Renal excretion:
•Active tubular secretion
It occurs in the proximal tubules.
The drug combines with a specific protein to pass through
the proximal tubules.
When a drug has a competitive reactivity to the protein that is
responsible for active transport of another drug .This will reduce
such a drug excretion increasing its con. and hence its toxicity.
EX., Probenecid ….. Decreases tubular secretion of
methotrexate.
21. * Passive tubular reabsorption;
Excretion and reabsorption of drugs occur in the tubules
By passive diffusion which is regulated by concentration
and lipid solubility.
Ionized drugs are reabsorbed lower than non-ionized ones
Ex1., Sod.bicarb. Increases lithium clearance
and decreases its action
Ex2., Antacids Increases salicylates
clearance and decreases its
action
22. It means alteration of the dug action without change in its
serum concentration by pharmacokinetic factors.
EX., Propranolol + verapamil Synergistic or additive
effect
Additive effect : 1 + 1 =2
Synergistic effect : 1 +1 > 2
Potentiation effect : 1 + 0 =2
Antagonism : 1-1 = 0
23. • Receptor interaction
• Competitive
• Non-competitive
• Sensitivity of receptor
• Number of receptor
• Affinity of receptor
• Alter neurotransmitter release /drug transportation
• Alter water/electrolyte balance
24. • Grapefruit juice and Terfenadine
• Grapefruit juice and cyclosporin
• Grapefruit juice and felodipine
• Grapefruit contains : furanocoumarin compounds
that can selectively inhibit CYP3A4
25. Pharmacology + Genetics/Genomics
• The study of how individual’s genetic inheritance
affects the body’s response to drugs (efficacy &
toxicity)
• The use of genetic content of humans for drug
discovery
26. Variations in drug response and drug
toxicity may result from
Variation in drug
transporters
• P-glycoprotien
Variation in disease
modifying genes
• Apolipoprotein (APOE)
Variation in drug
metabolizing
enzymes
• Cytochromes
P450
• Thiopurine S-methyltransferase
Variation in drug
targets
•Beta2-adrenergic
receptor
27. Dose related events may be managed by changing the
dose of the affected medicine.
• Eg.,when miconazole oral gel causes an increase in
bleeding time of warfarin then redusing the warfarin dose
will bring the bleeding time back into range and reduse
the risk of haemorrhage
• It is important to retitrate the dose of warfarin when the
course of miconazole is coumplete.
28. The potential severity of some interaction require
immediate
Cessation of the combination.
• Eg,.the combination of erythromycin and terfenadine can
produse high terfenadine level with the risk of developing
Torsel de Points.
Dose spacing is appropriate for interction involving the
inhibition of absorption in the GI tract .
• Eg.,avoidig the binding of ceprofloxacin by ferous salts
29.
30. No. Interaction between Number in 413
cases of
interactions
Percentage in
413 cases of
interactions
1 Ciprofloxacin-
Sucralfate
137 33.17
2 Ciprofloxacin-
Magnesium sulfate
22 5.32
3 Digoxin-
Metoclopramide
17 4.11
4 Theophylline- Rifampin 16 3.87
31. • Among the mechanisms of pharmacokinetic interactions,
the most dominant type was metabolic interaction with a
total percentage of %60.05.
• Table 2. Distribution of different mechanisms of the
pharma-cokinetic interactions
Mechanism Total number percentage
Metabolism 248 60.05
Absorption 158 38.26
Elimination 4 0.97
distribution 3 0.72
32. Interaction type Number of interaction Percentage
Onset
Delayed 251 61%
Rapid 162 39%
Severity
Major 72 17.43%
Moderate 335 73.61%
Minor 0 0%
Unknown 37 8.96%
Documentation
Establised 102 24.7%
Probable 166 39.95%
Suspected 109 26.39%
Unknown 37 8.96%
Significance
1 72 17.43%
2 335 73.61%
Unknown 37 8.96%
33. • Whenever a patient receives multiple drug therapy, the
possibility of a pharmacokinetic interaction exists.
• This study shows the most prevalent pharmacokinetic
interactions in ICU may be metabolic and those related
to absorption alterations (about %98.31).
• Interaction between ciprofloxacin and sucralfate, an
absorption type, was the most prevalent one .
• In the ICU, nurses usually determine timing of drug
administration.
34. • Study showed the higher the number of drugs in
prescriptions, the higher the number of interactions.
Therefore, polypharmacy should be avoided as much as
possible .
35. • Text book of Clinical pharmacy by Parth sarthi.
• K.D.Tripathi
• Iranian journal of p’ceutical research .page 215-218,2006
by school of pharmacy shahid baneshti university of
medical science and health services.