Detailed information of all terms like Thyroid gland, Thyroxine, Triidothyronine, Calcitonine, growth and development , propylthiouracil, Calorigenesis, tadpole to frog, Oligomenorrhoea, snehal chakorkar, pharmacology, Cretinism, Myxoedema coma, Graves disease, Thiocynates, Perchlorate, Nitrates.
Radioactive iodine, I131
Detailed information of all terms like Thyroid gland, Thyroxine, Triidothyronine, Calcitonine, growth and development , propylthiouracil, Calorigenesis, tadpole to frog, Oligomenorrhoea, snehal chakorkar, pharmacology, Cretinism, Myxoedema coma, Graves disease, Thiocynates, Perchlorate, Nitrates.
Radioactive iodine, I131
Autacoids - pharmacological actions and drugs related to them. SIVASWAROOP YARASI
Autacoids or "autocoids" are biological factors which act like local hormones, have a brief duration, and act near the site of synthesis. The word autacoids comes from the Greek "autos" (self) and "acos" (relief, i.e. drug).
This is an overview of drugs used to control nausea and vomiting. This presentation was for 2nd year pharmacy students as part of a pharmacology & toxicology course and accompanies Goodman & Gilman's (12e) chapter 46.
Autacoids - pharmacological actions and drugs related to them. SIVASWAROOP YARASI
Autacoids or "autocoids" are biological factors which act like local hormones, have a brief duration, and act near the site of synthesis. The word autacoids comes from the Greek "autos" (self) and "acos" (relief, i.e. drug).
This is an overview of drugs used to control nausea and vomiting. This presentation was for 2nd year pharmacy students as part of a pharmacology & toxicology course and accompanies Goodman & Gilman's (12e) chapter 46.
Lecture slides for MBBS Undergraduate Medical students. Study material was taken from Essentials of pharmacology by KD Tripathi. Figures were searched from google.
Emetics & Anti-emetics presentation for pharmacy studentsLokesh Patil
Emetics and antiemetics are drugs used to induce and prevent vomiting, respectively. Emetics, such as ipecac syrup and apomorphine, stimulate the vomiting center in the brain or irritate the stomach lining to induce vomiting, often used in cases of poisoning. Antiemetics, including drugs like ondansetron, metoclopramide, and promethazine, work by blocking neurotransmitters like serotonin, dopamine, and histamine, which are involved in triggering the vomiting reflex. They are commonly used to treat nausea and vomiting caused by conditions such as motion sickness, chemotherapy, and postoperative recovery. Understanding the mechanisms and applications of these drugs is crucial for effectively managing emesis in various clinical scenarios.
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
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Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
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2 Case Reports of Gastric Ultrasound
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
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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
9. Emetic Drugs - Uses
• Acute cases of poisoning (except in corrosive substances
poisoning or if patient is not fully conscious)
• Alcoholic intoxication
• Removal of foreign bodies from the oesophagus
• Certain cases of paroxysmal tachycardia
13. Manikandan 13
Apomorphine
• Semi synthetic derivative of morphine
• Given IM or SC, act centrally; local effect on GIT not required.
• Dose is 6 mg (2-8mg)
• Induces vomiting in 5 -10 min
• CNS depressant contraindicated in respiratory depression
•
14. Manikandan 14
Ipecacuanha
• Contains two alkaloids- emetine & cephaeline
• Used as syrup ipecac.
• Produces effect in 15 min.
• Acts by irritating gastric mucosa & through CTZ centre.
• Dose = 5ml in infants
= 10-15ml in children
= 15-20ml in adults
17. Manikandan 17
Introduction - Anti-emetics
• Two centres: vomiting centre (VC) and chemoreceptor
trigger zone (CTZ)
• Both near the floor of the fourth ventricle, close to the
vital centres
• VC is within the blood brain barrier (BBB)
• CTZ outside in the area postrema
• They are connected together
18. ANTIEMETIC
DRUGS
A group of drugs which are used to control
nausea and vomiting
Provide symptomatic relief
Removal of causative factor to have ultimate relief
19. Manikandan 19
Vomiting Centre
(medulla)
Cerebral cortex
Anticipatory emesis
Smell
Sight
Thought
Vestibular
nucleiMotion
sickness
Pharynx & GIT
Chemo & radio therapy
Gastroenteritis
Chemoreceptor
Trigger Zone
(CTZ)
(Outside BBB)
Cancer chemotherapy
Opioids
Muscarinic, 5 HT3
& Histaminic H1
5 HT3
receptors
Dopamine D2
5 HT3,
Opioid Receptors
Muscarinic
Histaminic H1
Pathophysiology of Emesis
23. D2 Antagonists
a. Substituted Benzamides
Metoclopramide, Trimethobenzamide
b. Butyrophenones
Domperidone , Droperidol
c. Phenothiazines
Prochlorperazine, Promethazine &
Thiethylperazine.
24. Metoclopramide
Chemistry: Substituted Benzamide
MOA: Dopamine D2 receptors antagonist
It is potent Antiemetic & Prokinetic agent
As Antiemetic
• It has potent Antiemetic & antinausea effect.
• Blocks D2 receptors in CTZ of the medulla (area postrema)
As Prokinetic agent
• It can selectively stimulate gut motor function.
• Blocks D2 receptor in GIT & blocks the normal inhibitory
effect of Dopamine on cholinergic smooth muscle
stimulation--- ↑ motility.
25. Manikandan 25
The Uses - Metroclopramide
Potent antiemetic controls / reduces vomiting due to
• Uremia
• Radiation
• Viral gastro enteritis, hepatic-biliary disease
• Anticancer drugs
• Migraine
• Post operatively & pre-operatively
26. Manikandan 26
Metroclopramide…
Pharmacokinetics
• Rapidly absorbed from GIT after oral administration.
• Undergoes a high degree first pass metabolism.
• It is excreted in the urine as free and as metabolites.
• It is also excreted in the breast milk.
• DOSE: 10-20mg orally or IV every 6 hrs
27. Adverse Effects - Metroclopramide
• Extrapyramidal reactions with facial and skeletal muscle
spasms- Restlessness, Dystonias , Parkinsonian symptoms.
-----More common in young and very old. Usually occur shortly
after staring treatment and subside with in 24 hours of stopping
the drug.
• Bowel upsets, Diarrhea
• Drowsiness and fatigue, dizziness, restlessness and anxiety.
• Galactorrhoea, Gynecomastia, impotence and menstrual
disorders – due to increased prolactin levels
29. Manikandan 29
Phenothiazines
Phenothiazines
Prochlorperazine, Promethazine & Thiethylperazine
Phenothiazines are antipsychotics with potent antiemetic
property due to D2 antagonism and anti-maucarinic
properties
Sedative property due to anti-histaminic property
Mainly used as anti-emetic in severe N& V
Main A/E: EPS , sedation , postural hypotension
30. Manikandan 30
Butyrophenones
Antipsychotic drugs , D2 antagonists
Droperidol
Central D2 antagonist
Main A/E: EPS , postural hypotension
QT prolongation may occur
Domperidone
• Does not cross BBB. Only blocks D2 in CTZ where BBB is leaky.
• May be used in N&V due to Levodopa, without affecting its
efficacy.
• No EPS.
• Used as antiemetic , prokinetic agent & for post partum lactation
stimulation.
31. Selective 5-HT3 Antagonists
Ondansetron, Granisetron , Dolasetron & Palonosetron
MOA
Act as anti-emetic by Selectively blocking central 5HT3 receptors in
Vomiting center & CTZ & Mainly by blocking Periphery 5HT3
receptors on intestinal vagal and spinal afferent fibers
Antiemetic action is restricted to emesis caused by vagal stimulation
(e..g post operative) & chemotherapy
Palonosetron: newer with greater affinity for 5-HT3 receptor &
comparatively longer half life
No effect on Dopamine / muscarinic receptors
32. Manikandan 32
Ph. K - Selective 5-HT3 Antagonists
• High first pass metabolism
• t1/2 : 4-9 hrs (Ondansetron, Granisetron & Dolasetron)
40 hrs (Palonosetron)
• Given once or twice daily – orally or intravenously
• Excreted by liver & kidney
• No dose reduction in renal insufficiency but needed in
hepatic insufficiency (Ondansetron)
33. Manikandan 33
The Uses - Selective 5-HT3 Antagonists
• Chemotherapy- Induced Nausea & vomiting
• Primary Agents - prevention of acute chemotherapy induced
Nausea & vomiting
Effective alone in most of the cases. Efficacy is enhanced in
combination. Can be given I/V 1/2 hr before chemotherapy
• To prevent Delayed Nausea & vomiting occurring after 24 hrs
of Cancer chemotherapy
in combination with Dexamethasone & NK1 receptor
antagonist.
• To prevent & treat post operative & post radiation
Nausea & vomiting
34. Manikandan 34
A/Es - Selective 5-HT3 Antagonists
• Excellent safety profile
• Headache, Dizziness & constipation
• All three drugs cause prolongation of QT interval, but
more pronounced with dolasetron.
DIs
Hepatic clearance may decrease by enzyme inhibitors
35. Manikandan 35
H1antihistamines & Muscarinic Antagonists
H1antihistamines
Meclizine, Cinnarizine, Cyclizine & Diphenhydramine &
its salt Dimenhydrinate.
• They have anticholinergic & H1 antagonist sedating properties
(1st generation).
• They produce specific depression of conduction in
vestibulocerebellar pathway.
MuscarinicAntagonist
Hyoscine (Scopolamine).
36. Manikandan 36
H1antihistamines & Muscarinic Antagonists…
Theraputic Uses
• Vestibular system is important in motion sickness
via cranial nerve VIII - rich in Cholinergic M1 &
Histamine H1receptors
• Most effective drugs for motion sickness
• Effective for nausea & vomiting associated with motion
sickness.
• Vestibular disorders ( Meniere’s disease)
• (hyoscine) – used as transdermal patch for motion sickness
• Meclozine is long acting so useful in sea sickness
• Cinnarizine also has antivertigo effect. Act by inhibiting
influx of calcium to vestibular sensory cells from
endolymph
38. • MOA: Act as antiemetic & appetite stimulant in addition
to psychoactive action. MOA not clear.
• Cancer chemotherapy induced Nausea & vomiting
with Phenothiazines – synergistic effect but AEs
are added – not used as better drugs are available
• Nabilone
• closely related THC analog
41. Neurokinin-1 (NK1 )Antagonists
Aprepitant, Fosaprepitant
Given orally BA = 65% , Crosses BBB.
t ½ : 11 hrs, Metabolized by hepatic CYP3A4.
MOA
Act as Antiemetic: Selectively block NK1 receptor in area
postrema.
No effect on Serotonin , Dopamine or Corticoid receptors
42. Manikandan 42
Aprepitant
• Non peptide, selective, Neurokinin type 1 (NK 1)
receptors antagonist
• Block substance P from binding to NK1 receptor
• Broader spectrum and activity in delayed emesis (In
Preclinical studies)
• Augment the antiemetic activity of 5HT3 receptor
antagonists and dexamethasone
• Inhibit both acute and delayed CINV
43. Manikandan 43
Neurokinin-1 (NK1 )Antagonists
Uses
Used in combination with 5HT3 antagonists &
Corticosteroids for prevention of acute & chronic
nausea and vomiting from Cancer chemotherapy
44. Manikandan 44
Neurokinin-1 (NK1 )Antagonists
A/Es
• Fatigue, dizziness & diarrhoea.
• Enzyme inhibition
• Metabolized by CYP3A4 & may inhibit metabolism of many anticancer drugs
(Docetaxel, Paclitaxel, Etoposide, Vinblastine, Imatinib) ---- ↑ levels ---
toxicity.
• Metabolism of Aprepitant may be inhibited by Ketoconazole, Ciprofloxacin,
Clarithromycin, Nafazodone, Ritonavir, Nelfinavir, Verapamil & Quinidine)
• Aprepitant ↓ INR in patients taking warfarin.
45. Manikandan 45
Therapeutic Uses of Anti-emetics
• Motion sickness: Hyoscine
• Vestibular disorders( Menieres, disease): Cinnerazine
• Vomiting due to Uremia, Radiation, Viral gastro enteritis,
Liver disease, Migraine, Prochlorperazine ,
Metroclopramide
• Vomiting due to pregnancy ( hyperemesis gravidarum),
Meclizine with vit. B6 (Navidoxine)
46. Manikandan 46
• Vomiting due to Cytotoxic Anticancer drugs: 5HT3
Antagonists Metroclopramide, Cannabinoids,
corticosteroids , Aprepitant
• Anticipatory Vomiting due to Cytotoxic Anticancer
drugs. Benzodiazepines (Diazepam)
• Post Operative Vomiting: Metoclopramide ,
Prochlorperazine , Dimenhydrinate, 5HT3 Antagonists
(Ondensetron)