The document summarizes the mechanism of nausea and vomiting. It discusses that nausea and vomiting are protective reflexes against toxins. The vomiting center in the medulla integrates afferent signals and coordinates the vomiting reflex. The vomiting center can be stimulated through irritation in the gastrointestinal tract, signals from the chemoreceptor trigger zone, stimulation of the vestibular system, or from higher brain centers. When stimulated, the vomiting center initiates the motor pathways that lead to nausea, salivation, and the expulsion of gastric contents through vomiting.
Slide set for medical students discussing the physiology and pharmacology of nausea and vomiting. Provided by Professor John A Peters, University of Dundee.
Nausea is an unpleasant sensation which is subjective and is different from one person to another person.
A person suffering from nausea also face
Pallor
Increased respiratory rate
salivation.
Retching :Rythmatic synchronized contractions of the diaphragm , abdominal and intercostal muscles against a closed glottis causing the intra abdominal and decrease the intra thoracic pressure causing the gastric contents to go up through the esophagus.
Vomiting is the process, emesis or throwing out, expulsion of stomach contents via esophagus and mouth.
Slide set for medical students discussing the physiology and pharmacology of nausea and vomiting. Provided by Professor John A Peters, University of Dundee.
Nausea is an unpleasant sensation which is subjective and is different from one person to another person.
A person suffering from nausea also face
Pallor
Increased respiratory rate
salivation.
Retching :Rythmatic synchronized contractions of the diaphragm , abdominal and intercostal muscles against a closed glottis causing the intra abdominal and decrease the intra thoracic pressure causing the gastric contents to go up through the esophagus.
Vomiting is the process, emesis or throwing out, expulsion of stomach contents via esophagus and mouth.
this presentation gives the knowledge about the decongestants are a type of medication that can provide short relief for a blocked nose ................
this presentation gives the knowledge about the decongestants are a type of medication that can provide short relief for a blocked nose ................
Side effects of chemotherapy are the most dreaded of all times. Fortunately, there are different ways to prevent, treat and manage the side effects today, and cancer specialists take special care to make sure that their patients don’t suffer.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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
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
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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
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
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- 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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
2. Mechanism of Nausea and Vomiting
1 | P a g e
Table of Contents
Background ................................................................................................................................................. 2
Etiology ........................................................................................................................................................ 2
Pathophysiology ......................................................................................................................................2-5
Management ...........................................................................................................................................5-6
Conclusion .................................................................................................................................................. 6
Refernces .................................................................................................................................................... 6
3. Mechanism of Nausea and Vomiting
2 | P a g e
—
Background
Nausea and vomiting are basic human protective reflexes against the absorption of toxins, as
well as responses to certain stimuli.9 Vomiting is the means by which the upper gastrointestinal
tract rids itself of its contents when almost any part of the upper tract becomes excessively
irritated, overdistended, or even overexcitable. Nausea which is often a prodrome of vomiting,
and is the conscious recognition of subconscious excitation in an area of the medulla closely
associated with or part of the vomiting center.1 And the aim of this paper, is to understand what
nausea and vomiting is? And how does it occur? Which is based on several references, both
medical books and articles.
Etiology
The main etiologies for nausea and vomiting include iatrogenic, that is almost any
medication that can cause nausea and vomiting, such as, chemotherapeutic agents. Toxic
infectious causes, which is mainly caused by ingestion of a toxin. The other causes contain
gastrointestinal disorders, central nervous system or psychiatric conditions, and some conditions
caused by metabolism such as Pregnancy, which is the most common endocrinologic cause of
nausea and vomiting. 2
Pathophysiology
There are many conditions out there that cause nausea and vomiting, but we know that there
are at least three kinds of nausea and vomiting, the first of which has been attributed to
anaesthetics such as ether, the second to reflex responses, the last to opioids. 8
Nausea and vomiting occurs via different mechanisms and pathways. The afferent and
efferent reflexes involved in nausea and vomiting are integrated with two distinct centers at
brainstem level, which are the vomiting center, where it is proposed that, it is multiple distributed
nuclei located in the medulla, that contain histamine (H1), acetylcholine (ACh) and
5hydroxytryptamine2 (5HT2) receptors, however, it is now thought that an anatomically discrete
vomiting center is unlikely to exist, as proposed nearly 60 years ago by Wang and Borison.
Rather, a number of loosely organized neuronal areas within the medulla probably interact to
coordinate the emetic reflex, and the neurons coordinating the complex series of events that
occur during emesis have been termed the “central pattern generator”.6 And the second center is
chemoreceptor trigger zone (CTZ), which is located bilaterally on the floor of the fourth
ventricle in area postrema near the obex, where this part has no blood-brain barrier and may be
accessible to humoral stimuli in either blood or cerebrospinal fluid, so various drugs, toxins and
metabolites can access it, and has dopamine (D2), 5HT3 and Neurokinin-1 receptors. The
vomiting center receives afferent stimulation via the CTZ, the cerebral cortex, and the vestibular
system, and peripheral stimulation via the vagal and sympathetic nerves which, in turn, leads to
emesis.
4. Mechanism of Nausea and Vomiting
3 | P a g e
Once the vomiting center stimulated, the vomiting reflex occurs which is divided into two
phases: (1) Pre-ejection phase, which is characterized by a sensation of nausea associated with
cold, sweating, pupil dilatation, salivation and tachycardia mediated by sympathetic and
parasympathetic nerves, (2) Ejection phase, where it comprises of retching and vomiting with
expulsion of gastric contents.
Nausea Which is the prodrome of vomiting, is excitation of part of the medulla that is
closely associated with vomiting center, which can be caused by (1) irritative impulses coming
from the gastrointestinal tract, (2) impulses that originate in the lower brain associated with
motion sickness, or (3) impulses from the cerebral cortex to initiate vomiting. But it doesn’t
mean that Nausea and Vomiting are coupled together, because vomiting can occasionally occur
without the prodromal sensation of nausea, indicating that only certain portions of the vomiting
center area associated with the sensation of nausea. Vomiting usually starts with salivation and
the sensation of nausea, and the vomiting reflex occurs only when through stimulation of the
vomiting center.
There are several ways that vomiting center is stimulated, the First way is when the stomach
and the upper portions of the small intestine faces irritation, excessive distention or
overexcitation, it causes antiperistalisis -the prelude of vomiting-, often appears many minutes
before vomiting, which is peristalsis up the digestive tract rather than downward. This may begin
as far down in the intestinal tract as the ileum, and the antiperistaltic wave travels backward up
the intestine at a rate of 2 to 3 cm/sec; this process can actually push a large share of the lower
small intestine contents all the way back to the duodenum and stomach within 3 to 5 minutes.
Then, as these upper portions of the gastrointestinal tract, especially the duodenum, become
overly distended, this distention becomes the
exciting factor and an impulse is formed by
stimulation of H1 and ACh receptors, leading to an
afferent stimulus that terminates in the brain stem by
both vagal and sympathetic afferent nerve fibers,
primarily in the nucleus tractus solitarius, and
subsequently activates the vomiting center, which is
shown in figure (1).
The emetic stimuli in gut are detected by two types
of vagal afferent fibres, mechanoreceptors and
chemoreceptors, and the abdominal vagal afferents
appear to have the greatest relevance for
chemotherapy-induced nausea and vomiting, and
post-operative nausea and vomiting.
Second way is arising nervous signals in
chemoreceptor trigger zone. Electrical stimulation
and administration of certain drugs, including
apomorphine, morphine, and some digitalis
derivatives, can directly stimulate this
chemoreceptor trigger zone and in return stimulating
Vomiting center, as shown in figure(1). Destruction
of this area blocks this type of vomiting but does not
block vomiting resulting from irritative stimuli in the
gastrointestinal tract itself.
5. Mechanism of Nausea and Vomiting
4 | P a g e
Third way, is through stimulation of Ach or H1 receptors in the vestibular labyrinth of the
inner ear, when direction or rhythm of motion of the body is changed, which then transmitted to
vestibular nuclei that mediates the nausea and vomiting of motion sickness, from there, it is
transmitted into the cerebellum, then to the chemoreceptor trigger zone, and finally to the
vomiting center to cause vomiting.
Fourth way is stimulation of the Vomiting
Center from higher centers of the brain. When a
stimulation is formed from the diencephalon,
limbic system and cerebral cortex, then
transmitted to the cortical center, after that to
vomiting center to cause vomiting. Because
emetic responses to emotionally charged
stimuli such as nauseating smells, sickening
sights and pain occur. In addition to the
pathways already described, when there is
raised intracranial pressure cerebral histamine
receptors may be stimulated and meningeal
mechanoreceptors stimulate the vomiting
center. Also vestibular cardiac afferent induce
nausea and vomiting as in MI, and pharyngeal
stimulation may induce nausea and vomiting,
too. Figure (2) demonstrates the most of the
pathways for the stimulation of the vomiting
center, which we talked about before.9
Once the vomiting center has been
sufficiently stimulated and the vomiting act
instituted, the vomiting act takes place, where
motor impulses that cause the actual vomiting
are transmitted from the vomiting center by
way of the 5th, 7th, 9th, 10th, and 12th cranial nerves to the upper gastrointestinal tract, through
vagal and sympathetic nerves to the lower tract, and through spinal nerves to the diaphragm and
abdominal muscles, which cause the following effects that are (1) a deep breath, (2) raising of
the hyoid bone and larynx to pull the upper esophageal sphincter open, (3) closing of the glottis
to prevent vomitus flow into the lungs, and (4) lifting of the soft palate to close the posterior
nares. Also Serotonin (5-HT) released from enterochromaffin cells in the small intestine that
initiate impulses via 5-HT 3 receptors trigger vomiting, where reverse peristalsis empties
material from the upper part of the small intestine into the stomach, and it causes distention of
the stomach, which means further stimulation of the vomiting center. Next comes a strong
downward contraction of the diaphragm along with simultaneous contraction of all the
abdominal wall muscles, along with partial relaxation of the esophageal-stomach sphincter, thus
allowing vomitus to begin moving from the stomach into the esophagus. This squeezes the
stomach between the diaphragm and the abdominal muscles, building the intragastric pressure to
a high level. Finally, the lower esophageal sphincter relaxes completely, allowing expulsion of
the gastric contents upward through the esophagus, then the vomitus is expelled to the exterior
easily. 1, 4,6,8 The vomiting act is simply shown in Figure (3). 7
6. Mechanism of Nausea and Vomiting
5 | P a g e
Management
A wide variety of antiemetic agents are available for the prevention and treatment of nausea and
vomiting. These agents can be classified according to the therapeutic index of their usefulness as
high index, such as, 5-HT3 antagonists or low index, such as, cannabinoids. The table below
shows some common antiemetic agents.
Class of medication Example Common uses
Antihistamines cyclizine Possible adjunct for cytotoxic
chemotherapy, prophylaxis
and treatment of motion
sickness
Butyrophenones droperidol Anticipatory and acute
chemotherapeutic nausea and
vomiting, postoperative
nausea and vomiting
Cannabinoids dronabinol Refractory chemotherapy-
related nausea and vomiting
Corticosteroids dexamethasone Adjunct for chemotherapy
related symptoms
5-HT3 Antagonists dolasetron Post chemotherapy nausea and
vomiting, severe nausea and
vomiting
7. Mechanism of Nausea and Vomiting
6 | P a g e
There are also alternative treatments such as, Acupuncture, Acupressue, Ginger (powdered root),
and Pyridoxine for conditions like, chemotherapy-induced nausea and vomiting, post-operative
nausea and vomiting and early pregnancy nausea and vomiting.2,7
Conclusion
After over 150 years of research, still the mechanism of nausea and vomiting is not very clear?.
there are four factors that help us answer this ‘million’ dollar question: the First factor is
complexity of the problem, due to the variables which are so many that it becomes difficult to
identify the mechanism to assess the effects of an intervention, as it requires a considerable
number of patients in well controlled trials. Second is lack of animal model to study the
physiology and pharmacology of the mechanism of nausea and vomiting. Many species, such as,
rat and rabbit do not vomit irrespective of stimulus. Though, monkeys and dogs respond to the
same range of emetic stimuli as man with cytotoxic drugs and radiation, they do not suffer from
pregnancy and motion sickness and post-operative and post-anaesthetic emesis. The last factor is
inadequate quantification of the phenomena, irrespective of the huge number of clinical trials,
the phenomena have been poorly quantified. 8
References
1. Guyton AC, Hall JE. Gastrointestinal Physiology. Textbook of Medical Physiology 11th
ed. P823.
2. Scorza K, Williams K, Phillips JD, Shaw J. Evaluation of Nausea and Vomiting.
American Family Physician, 2007. V76, N1, P76-7.
3. Einarson TR, Piwko C, Koren G. Prevalence of Nausea and Vomiting of pregnancy in the USA.
University of Toronto.
4. Barrett KE, Boitano S, Barman SM, Brooks HL. Gastrointestinal Physiology. Ganong’s
Review of Medical Physiology 24ed .P502.
5. Chand S. Nausea and vomiting in palliative care, 2014. The Pharmaceutical Journal.
P2,3.
6. Hesketh PJ. Chemotherapy-Induced Nausea and Vomiting. N Engl J Med
2008.358,2482-94.
7. Paulev PE, Calleja GZ. New Human Physiology 2nd ed. Gastrointestinal Function and
Disorders, Chap22.
8. Islam S, Jain PN. post-operative nausea and vomiting (PONV) : a review article. Indian J.
Anaesth, 2004.48(4):253-258.
9. Garrett K, Tsuruta K, Walker S, Jackson S, Sweat M. Managing Nausea and Vomiting.
Critical Care Nurse, 2003. V23, N1.