Nausea-vomiting By nader al-assadi Vomiting (emesis) is the oral expulsion of gastrointestinal contents due to gut and thoracoabdominal wall contractions. Nausea is the subjective feeling of a need to vomit. regurgitation, the effortless passage of gastric contents into the mouth. Rumination is the repeated regurgitation of food residue, which may be rechewed and reswallowed. In contrast to emesis, these phenomena exhibit volitional control. Indigestion is a term encompassing a range of complaints including nausea, vomiting, heartburn, regurgitation, and dyspepsia .

1. vomiting
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2. Outlines
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3. Definition
Vomiting (emesis) is the oral expulsion of gastrointestinal
contents due to gut and thoracoabdominal wall
contractions.
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4. Some terms related to vomiting
Nausea is the subjective feeling of a need to vomit.
regurgitation, the effortless passage of gastric contents into the mouth.
Rumination is the repeated regurgitation of food residue, which may be
rechewed and reswallowed. In contrast to emesis, these phenomena exhibit
volitional control.
Indigestion is a term encompassing a range of complaints including nausea,
vomiting, heartburn, regurgitation, and dyspepsia .
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5. Some terms related to vomiting
Postchemotherapy nausea and
vomiting (PCNV):3 types: acute, within 24 hours; delayed, after 24
hours later; and anticipatory,just before the next chemotherapy
dose.
Chronic nausea and vomiting The persistence of the symptoms for
> 1 month.
Early satiety :The sensation of feeling full after eating an
unusually small amount of food.
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6. MECHANISMS
•Vomiting is coordinated by the brainstem and is effected by responses in the gut, pharynx, and somatic
musculature.
•Mechanisms underlying nausea are poorly understood but likely involve the cerebral cortex, as nausea
requires conscious perception. This is supported by functional brain imaging studies showing activation of
cerebral cortical regions during nausea.
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7. Act of Vomiting
Act of vomiting involves series of movements that takes
place in GI tract.
Sequence of events:
1. Beginning of antiperistalsis, which runs from ileum
towards the mouth through the intestine, pushing the intestinal contents into the stomach within few
minutes. Velocity of the antiperistalsis is about 2 to 3 cm/second.
2. Deep inspiration followed by temporary cessation of
breathin
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8. Act of Vomiting
3. Closure of glottis
4. Upward and forward movement of larynx and hyoid
bone
5. Elevation of soft palate
6. Contraction of diaphragm and abdominal muscles
with a characteristic jerk, resulting in elevation of
intra-abdominal pressure
7. Compression of the stomach between diaphragm
and abdominal wall leading to rise in intragastric
pressure
8. Simultaneous relaxation of lower esophageal sphincter, esophagus and upper esophageal sphincter
9. Forceful expulsion of gastric contents (vomitus)
through esophagus, pharynx and mouth.
Movements during act of vomiting throw the vomitus
(materials ejected during vomiting) to the exterior
through mouth.
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9. Act of Vomiting
Some of the movements play important roles by preventing the entry of vomitus through other routes
and thereby prevent the adverse effect of the
vomitus on many structures. Such movements are:
1. Closure of glottis and cessation of breathing
prevents entry of vomitus into the lungs
2. Elevation of soft palate prevents entry of vomitus
into the nasopharynx
3. Larynx and hyoid bone move upward and forward
and are placed in this position rigidly. This causes
the dilatation of throat, which allows free exit of
vomitu
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10. VOMITING REFLEX
Activators of Emesis Emetic stimuli act at several sites.
Emesis evoked by unpleasant thoughts or smells originates in the brain.
 cranial nerves mediate vomiting after gag reflex activation
Motion sickness and inner ear disorders act on labyrinthine pathways
.Gastric irritants and cytotoxic agents like cisplatin stimulate gastroduodenal vagal afferent nerves. Nongastric afferents are
activated by bowel obstruction and mesenteric ischemia.
The area postrema, in the medulla, responds to bloodborne stimuli (emetogenic drugs, bacterial toxins, uremia, hypoxia,
ketoacidosis) and is termed the chemoreceptor trigger zone.
Neurotransmitters mediating vomiting are selective for different sites.
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11. VOMITING REFLEX
. Labyrinthine disorders stimulate vestibular muscarinic M1and histaminergic H1
receptors.
 Vagal afferent stimuli activate 5-HT3 receptors.
The area postrema is served by nerves acting on 5-HT3, M1, H1, and dopamine D2
subtypes.
Central NK1 receptors mediate both nausea and vomiting.
Cannabinoid CB1pathways may participate in the cerebral cortex and brainstem. Optimal
pharmacologic therapy of vomiting requires understanding these pathways.
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12. VOMITING
PATHWAYS
Ipecac syrup
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13. Causes and classification
of vomiting
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14. 1-accordeing to causes(infectious-non infectious).
2- according to protinieal/extraprotinal causes.
3- into local-systemic –central
4-According to associated symptoms.
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15. 1. Presence of irritating contents in GI tract
2. Mechanical stimulation of pharynx
3. Pregnancy
4. Excess intake of alcohol
5. Nauseating sight, odor or taste
6. Unusual stimulation of labyrinthine apparatus, as in
the case of sea sickness, air sickness, car sickness
or swinging
7. Abnormal stimulation of sensory receptors in other
organs like kidney, heart, semicircular canals or
uterus
8. Drugs like antibiotics, opiates, etc.
9. Any GI disorder
10. Acute infection like urinary tract infection, influenza,
etc.
11. Metabolic disturbances like carbohydrate starvation
and ketosis (pregnancy), uremia, ketoacidosis
(diabetes) and hypercalcemia
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16. Cause of
vomiting
infectiou
s
G.I.T
- H.pylori
Food
poising
G.E
Non G.I.T
meningiti
s
Pneumon
ia
malaria
Covid -19
Non
infectiou
s
G.I.T
Pyloric
stenosis.
All causes of
obstruction.
acute
cholecyst
itis
Alcoholic
hepatitis.
Non G.I.T
Acute
renal
failure
Chronic
renal
failure
Metaboli
c cause
truma
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17. 2-according to protinieal/extraprotinal causes
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18. Intraperitoneal Disorders
Visceral obstruction and inflammation of hollow and solid viscera may elicit vomiting.
Gastric obstruction results from ulcers and malignancy.
Small-bowel and colon blockage occur because of adhesions, benign or malignant tumors, volvulus,
intussusception, or inflammatory diseases like Crohn’s disease.
The superior mesenteric artery syndrome, occurring after weight loss or prolonged bed rest, results when the
duodenum is compressed by the overlying superior mesenteric artery.
Abdominal irradiation impairs intestinal motor function and induces strictures. Biliary colic causes nausea by
acting on local afferent nerves.
Vomiting with pancreatitis, cholecystitis, and appendicitis result from visceral irritation and induction of ileus.
Enteric infections with viruses like norovirus or rotavirus or bacteria like Staphylococcus aureus and Bacillus
cereus cause vomiting, especially in children.
Opportunistic infections like cytomegalovirus or herpes simplex virus induce emesis in immunocompromised
individuals.
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19. Cont.….
Gastroparesis presents with symptoms of gastric retention with evidence of delayed gastric emptying and
occurs after vagotomy or with pancreatic carcinoma, mesenteric vascular insufficiency, or organic diseases
like diabetes, scleroderma, and amyloidosis.
Idiopathic gastroparesis is the most common etiology. It occurs in the absence of systemic illness and
follows a viral illness in ~15–20% of cases, suggesting an infectious trigger.
Intestinal pseudoobstruction is characterized by disrupted intestinal and colonic motor activity with
retention of food residue and secretions; bacterial overgrowth; nutrient malabsorption; and symptoms of
nausea, vomiting, bloating, pain, and altered defecation.
Intestinal pseudoobstruction may be idiopathic, inherited as a familial visceral myopathy or neuropathy,
result from systemic disease like scleroderma or an infiltrative process like amyloidosis, or occur as a
paraneoplastic consequence of malignancy (e.g., small-cell lung carcinoma).
Patients with gastroesophageal reflux report nausea and vomiting, as do some with irritable bowel
syndrome (IBS) or chronic constipation.
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20. Cont.….
Other functional gastroduodenal disorders without organic abnormalities have been characterized.
Chronic nausea vomiting syndrome is defined as bothersome nausea at least one day and/or one
or more vomiting episodes weekly in the absence of an eating disorder or psychiatric disease.
Cyclic vomiting syndrome causes 3–14% of cases of unexplained nausea and vomiting and presents
with periodic discrete
episodes of relentless vomiting in children and adults and shows an association with migraine
headaches, suggesting that some cases may be migraine variants. Some adult cases have been
associated with rapid gastric emptying. A related condition, cannabinoid hyperemesis syndrome,
presents with cyclical vomiting with intervening well periods in individuals (mostly men) who use
large quantities of cannabis over many years and resolves with its discontinuation.
Pathologic behaviors such as taking prolonged hot baths or showers are associated with the
syndrome.
Rumination syndrome, characterized by repetitive regurgitation of recently ingested food, is often
misdiagnosed as refractory vomiting.
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21. Extraperitoneal Disorders
Myocardial infarction and congestive heart failure may cause nausea and vomiting. Postoperative emesis occurs
after 25% of surgeries, most commonly abdominal and orthopedic surgery.
Increased intracranial pressure from tumors, bleeding, abscess, or blockage of cerebrospinal fluid outflow
produces vomiting with or without nausea.
Patients with psychiatric illnesses including anorexia nervosa, bulimia nervosa, anxiety, and depression often
report significant nausea that may be associated with delayed gastric emptying.
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22. Medications and Metabolic Disorders
Drugs
evoke vomiting by action on the stomach (analgesics, erythromycin) or area postrema (opiates, anti-parkinsonian
drugs).
Other emetogenic agents include antibiotics, cardiac antiarrhythmics, antihypertensives, oral hypoglycemics,
antidepressants (selective serotonin and serotonin norepinephrine reuptake inhibitors), smoking cessation drugs
(varenicline, nicotine), and contraceptives.
Cancer chemotherapy causes vomiting that is acute (within hours of administration), delayed (after
1 or more days), or anticipatory.
Acute emesis from highly emetogenic agents (e.g., cisplatin) is mediated by 5-HT3
pathways.
Delayed emesis is less dependent on 5-HT3 pathways with greater mediation by NK1
mechanisms.
Anticipatory nausea may respond to anxiolytic therapy rather than antiemetics.
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23. Metabolic Disorders
most prevalent endocrinologic cause, and nausea affects 70% of women
in the first trimester.
Hyperemesis gravidarum is a severe form of nausea of pregnancy that produces significant dehydration and
electrolyte disturbances.
Uremia, ketoacidosis, adrenal insufficiency, and parathyroid and thyroid disease are other metabolic
etiologies.
Circulating toxins evoke emesis via effects on the area postrema.
Endogenous toxins are generated in fulminant liver failure, whereas exogenous enterotoxins may be
produced by enteric bacterial infection.
Ethanol intoxication is a common toxic etiology of nausea and vomiting.
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24. Clues to psychogenic vomiting
•Usually female and often young
•May deny or minimize nausea
•Rarely occurs in public or in front of others
•Co-existent eating disorder, laxative abuse, diuretic abuse common
•Psychological disturbances common
•Complications of vomiting may be present
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25. Surreptitious vomiting:
when to suspect it
•Unexplained weight loss
•Co-existent eating disorder or other psychological condition
•Co-existent laxative and/or diuretic abuse
•Electrolyte and/or acid-base disturbances consistent with vomiting, including hypo-kalemic
nephropathy.
•Emetic complications (with denial of vomiting)
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26. Local cause
Pyloric
stonosis
-Wrong fetus
positing
during breast
feeding
Achalasia
3- into local-systemic –central
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27. Centeral cause (the
most common )
Any problem in brain
steam
Meniere’s
diseases(disorder in
inner ear)
Headache
Margarine
3- into local-systemic –central
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28. Systemic causes
Metabolic
cause:
-DKA
-Hypercalcimia
-hypokalimia
Chronic renal
failure:
-Uremia cause
repeated
vomiting
Chronic liver
disease.
Addison
disease:
primary
adrenocortical
insuffecieny
3- into local-systemic –central
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29. 4-According to associated symptoms.
Vomiting with
abdominal pain with
fever
• GE,TB,meningitis.
• Splenic mesenteric
infarction
Vomiting with
abdominal pain –no
fever
• Pyloric
obestruciton(acidic)
• Post pyloric
obstruction(alkaline)
• Large bowel
obstruction (fecal bad
odour )
Vomiting no abdominal
pain with fever
• Any cause of increase
ICP.
• Meningitis
,encephalitis.
Vomiting no
abdominal pain –no
fever.
• Any thing cause
sever headache with
out fever.
• Eg :
embolus,truma,CVA
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30. Diagnosis
HISTORY AND PHYSICAL EXAMINATION
The history helps define the etiology of nausea and vomiting.
Drugs, toxins, and infections often cause acute symptoms.
established illnesses evoke chronic complaints. Gastroparesis and pyloric.
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31. HISTORY
Nausea and Vomiting:
Key Historical Questions
How long?
Relationship to meals?
Contents of vomitus?
Associated symptoms
◦ pain in chest or abdomen, fever, myalgias, diarrhea, vertigo, dizziness, headache, focal
neurological symptoms, jaundice, weight loss
Diabetes?
When was last menstrual period?
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32. HISTORY
•obstruction elicit vomiting within an hour of eating.
•Emesis from intestinal blockage occurs later.
•Vomiting occurring minutes after meal consumption prompts consideration of rumination syndrome.
•With severe gastric emptying delays, the vomitus may contain food residue ingested days before.
• Hematemesis raises suspicion of an ulcer, malignancy, or Mallory-Weiss tear. Feculent emesis is noted with distal intestinal or colonic
obstruction.
• Bilious vomiting excludes gastric obstruction, whereas emesis of undigested food is consistent with a Zenker’s diverticulum or achalasia.
•Vomiting can relieve abdominal pain from a bowel obstruction, but has no effect in pancreatitis or cholecystitis.
•Profound weight loss raises concern about malignancy or obstruction.
•Fevers suggest inflammation.
•intracranial source is considered if there are headaches or visual field changes.
•Vertigo or tinnitus indicates labyrinthine disease.
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33. EXAMINATION
Nausea and Vomiting:
Key Physical Findings
•Vital signs
•BP and pulse tilt test
•Cardiopulmonary exam
•Abdominal exam
•Rectal exam
•Neurological exam including funduscopic exam (papilledema)
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34. EXAMINATION
•Orthostatic hypotension and reduced skin turgor indicate intravascular fluid loss.
•Pulmonary abnormalities raise concern for aspiration of vomitus.
•Bowel sounds may be absent with ileus.
•High-pitched rushes suggest bowel obstruction, whereas a succussion splash upon abrupt
lateral movement of the patient is found with gastroparesis or pyloric obstruction.
• Tenderness or involuntary guarding raises suspicion of inflammation.
•Fecal blood suggests mucosal injury from ulcer, ischemia, or tumor.
•Neurologic disease presents with papilledema, visual field loss, or focal neural abnormalities.
Neoplasm is suggested by palpable masses or adenopathy.
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35. DIAGNOSTIC TESTING
Laboratory studies: guided by history and
physical
•Electrolytes, glucose, BUN/creatinine
•Calcium, albumin, total serum proteins
•CBC
•LFTs
•Pregnancy test
•Urinalysis
•Serum lipase  amylase
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36. DIAGNOSTIC TESTING
Radiology studies: guided by history
and physical
•Plain abdominal films
•Abdominal sono or CT if pain is key feature
•Head CT or MRI if severe headache, papill-edema, marked hypertension,
altered mental status, or focal neurological findings
•EGD or upper GI to separate GOO or high duodenal obstruction from
gastroparesis
•Radiopaque marker emptying studies or radionuclide scintigraphy, esp. if
diabetic
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37. DIAGNOSTIC TESTING
•For intractable symptoms or an elusive diagnosis, selected screening tests can direct clinical care. Iron-
deficiency anemia mandates a search for mucosal injury.
•Pancreaticobiliary disease is indicated by abnormal pancreatic or liver biochemistries.
• Endocrinologic, rheumatologic, or paraneoplastic etiologies are suggested by hormone or serologic
abnormalities.
•If obstruction is suspected, supine and upright abdominal radiographs may show intestinal air-fluid levels
with reduced colonic air. Ileus is characterized by diffusely dilated air-filled bowel loops.
•Anatomic studies may be indicated if initial testing is nondiagnostic. Upper endoscopy detects ulcers,
malignancy, and retained food residue in gastroparesis.
• Small-bowel barium radiography or computed tomography (CT) diagnoses partial bowel obstruction.
•Colonoscopy or contrast enema radiography detects colonic obstruction. Ultrasound or CT defines
intraperitoneal inflammation; CT and magnetic resonance imaging (MRI) enterography provide define
inflammation in Crohn’s disease. Brain CT or MRI can delineate intracranial disease.
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38. DIAGNOSTIC TESTING
•. Mesenteric angiography, CT, or MRI is useful for suspected ischemia.
•Gastrointestinal motility testing may detect an underlying motor disorder.
• Gastroparesis commonly is diagnosed by gastric scintigraphy, by which measures emptying of a
radiolabeled meal.
• A non-radioactive 13C-labelled gastric emptying breath test was FDA-approved in 2015 and may be a
cost-effective alternative to scintigtraphy. Intestinal pseudoobstruction is suggested by abnormal barium
transit and luminal dilation on small-bowel contrast radiography. Wireless motility capsule methods
measure transit in the stomach, small bowel, and colon by detecting pH changes between regions and
also can diagnose gastroparesis and small bowel dysmotility.
•Small-intestinal manometry can confirm the diagnosis of pseudoobstruction and characterize the motor
abnormality as neuropathic or myopathic based on contractile patterns.
•Manometry can obviate the need for surgical intestinal biopsy to detect smooth muscle or neuronal
degeneration.
•Combined ambulatory esophageal pH/impedance testing and high-resolution manometry facilitates
diagnosis of rumination syndrome. NADER AL-ASSADI

39. Treatment
•GENERAL PRINCIPLES
•Therapy of vomiting is tailored to correcting remediable abnormalities if possible.
•Hospitalization is considered for severe dehydration, especially if oral fluid replenishment cannot be sustained.
Once oral intake is tolerated, nutrients are restarted with low-fat liquids, because lipids delay gastric emptying. A
low residue, small particle diet has shown efficacy in gastroparesis in a controlled study.
• Controlling blood glucose in poorly controlled diabetics can reduce hospitalizations in gastroparesis and may
improve nausea and vomiting.
•Treat complications regardless of cause
e.g., replace salt, water, potassium losses
•. Identify and treat underlying cause, whenever possible.
•. Provide temporary symptomatic relief of the symptoms.
• Use preventive measures when vomiting is likely to occur (e.g., cancer chemotherapy, parenteral opiate
administration)
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40. Treatment
Nonpharmacologic Therapy:
Acupressure Wristbands
Devices such as the Sea-Band function by stimulating the pericardium 6 (P6) point on the forearm. They can be
useful in preventing N/V in a variety of conditions, such as pregnancy or motion sickness, where traditional
drug therapy may not be warranted or desired.
Vitamins/Herbals
A variety of botanical products have been advocated for use in N/V.
Ginger (Zingiber officinale) has some limited data to support use in pregnancy, motion sickness, and surgery.[
Ginger does not produce central nervous system (CNS) depression, and may be an alternative to
antihistamines.
Peppermint (Mentha piperita), chamomile (Matricaria recutita), and lemon balm (Melissa officinalis) are
thought to have antispasmodic properties that may be helpful in treating N/V.
Vitamin B6 (pyridoxine) has also been advocated for use in pregnant women experiencing N/V and is included
in the recently approved product Diclegis (doxylamine-pyridoxine).
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41. Treatment
•ANTIEMETIC MEDICATIONS
•Antihistamines like dimenhydrinate and meclizine and anticholinergics like scopolamine act on
labyrinthine
•pathways to treat motion sickness and labyrinthine disorders.
• D2antagonists treat emesis evoked by area postrema stimuli and are used for medication,
toxic, and metabolic etiologies. Dopamine antagonists cross the blood-brain barrier and cause
anxiety, movement disorders, and hyperprolactinemic effects (galactorrhea,
•sexual dysfunction).
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42. Treatment
• 5-HT3antagonists like ondansetron and granisetron prevent postoperative vomiting, radiation
therapy–induced symptoms, and cancer chemotherapy–induced emesis, but also are used for
other causes of emesis.
• NK1antagonists like aprepitant are approved for chemotherapy-induced vomiting and also
reduce gastroparesis symptoms.
•Tricyclic antidepressants reduce symptoms in some patients with functional causes of
vomiting, but did not show benefits in a controlled trial in gastroparesis.
•Other antidepressants such as mirtazapine and olanzapine and the pain-modulating agent
gabapentin also may exhibit antiemetic effects.
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43. Treatment
•GASTROINTESTINAL MOTOR STIMULANTS
•Drugs that stimulate gastric emptying are used for gastroparesis Metoclopramide, a combined 5-HT4
• agonist and D2antagonist, is effective in gastroparesis, but antidopaminergic side effects, including
dystonias and mood disturbances, limit use in ~25% of cases.
• Erythromycin increases gastroduodenal motility by action on receptors for motilin, an endogenous
fasting motor stimulant.
• Intravenous erythromycin is useful for inpatients with refractory gastroparesis.
•Domperidone, a D2antagonist, exhibits prokinetic and antiemetic effects but does not cross into most
brain regions; thus, dystonic reactions are rare.
• Domperidone can induce hyperprolactinemic side effects via effects on pituitary regions served by a
porous blood-brain barrier. Prucalopride, a 5-HT4agonist available in Canada and Europe, has shown
efficacy in a preliminary gastroparesis trial.
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44. Treatment
• Intestinal pseudoobstruction may respond to the somatostatin analogue octreotide, which induces propagative small-
intestinal motor complexes.
•Acetylcholinesterase inhibitors like pyridostigmine may benefit some patients with small-bowel dysmotility.
• Pyloric botulinum toxin injections are reported in uncontrolled studies to reduce gastroparesis symptoms, but small
controlled trials observe benefits no greaterthan sham treatments.
• Surgical pyloroplasty and peroral endoscopic myotomy (POEM) of the pylorus has improved symptoms in case series.
• Placing a feeding jejunostomy reduces hospitalizations and improves overall health in some patients with refractory
gastroparesis.
• Postvagotomy gastroparesis may improve with near-total gastric resection; similar operations are being tried for
other gastroparesis etiologies.
•Implanted gastric electrical stimulators may reduce symptoms, enhance nutrition, improve quality of life, and
decrease health care expenditures in medication-refractory gastroparesis, but small controlled trials do not report
convincing benefits.
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45. When to Refer a Patient?
•Patients should be referred when presenting with severe or alarm symptoms such as signs of
dehydration, fever, bloody vomitus, jaundice, changes in vision, severe headache, or neck pain. If
a patient’s medical history includes asthma, chronic bronchitis, or emphysema, the patient may
react adversely to OTC treatments and should be referred. If a pharmacist suspects that a
patient’s N/V is related to anorexia or bulimia, he or she should ensure that the patient receives
appropriate counseling by a trained professional. If poisoning is suspected.
•Another patient presentation that requires referral is N/V due to a chronic condition, such as
gastroparesis and refractory or prolonged N/V. Symptoms persisting longer than 1 week after an
appropriate intervention is made could indicate a more serious etiology and should be referred
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46. Summary in treatment
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47. Drugs with anti- emetic prop-erties and known mechanisms
Antihistamines, e.g., meclizine (AntivertR)
◦ esp. for vestibular disorders
Anticholinergics, e.g., scopolamine (Transderm ScopR, DonnatalR)
◦ esp. for vestibular and GI disorders
Dopamine antagonists, e.g.,metoclopramide (ReglanR) or prochlorperazine
(CompazineR)
◦ esp. for GI disorders
Selective serotonin-3 (5HT3) RAs, e.g., odansetron, granisetron, dolasetron
◦ esp. to prevent chemotherapy-induced nausea/vomiting
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48. Drugs with anti-emetic properties (continued)
Multiple mechanisms of action:
Promethazine (PhenerganR)
◦ dopamine antagonist
◦ H1 antihistamine
◦ anticholinergic
◦ CNS sedative
◦ prevention of opiate-induced nausea and vomiting
Hydroxyzine (AtaraxR, VistarilR)
◦ H1 antihistamine
◦ anticholinergic
◦ CNS sedation
◦ prevention of opiate-induced nausea and vomiting
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49. Drugs with anti-emetic
properties (continued)
Uncertain mechanism of action:
Trimethobenzamide (TiganR)
◦ blocks apomorphine-induced emesis in dogs
◦ does not block emesis from p.o. CuSO4 in dogs
 probably acts in the chemoreceptor trigger zone (CTZ) of the medulla oblongata
Bismuth subsalicylate (Pepto-BismolR)
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50. Adjunctive antiemetic agents
Dexamethasone (DecadronR)
◦ along with other anti-emetics for prevention of cancer chemotherapy-induced emesis
Dronabinol (MarinolR)
◦ for prevention of cancer chemotherapy-induced emesis refractory to other agents
◦ [ also for anorexia and weight loss in AIDS]
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51. SAFETY CONSIDERATIONS
•Safety concerns have been raised about selected antiemetics. Centrally acting antidopaminergics,
especially metoclopramide, can cause irreversible movement disorders like tardive dyskinesia,
particularly in older patients. This complication should be explained and documented in the medical
record.
•Domperidone, erythromycin, tricyclic antidepressants, and 5HT3antagonists can induce dangerous cardiac
arrhythmias, especially in those with QTc interval prolongation on electrocardiography (ECG).
• Surveillance ECG testing has been advocated for some of these agents.
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52. SELECTED CLINICAL SETTINGS
•Some cancer chemotherapies are intensely emetogenic Combining a 5-HT3antagonist, an
NK1antagonist, and a glucocorticoid can control both acute and delayed vomiting after highly
•emetogenic chemotherapy. Unlike other drugs in the same class,
•the 5-HT3antagonist palonosetron can prevent delayed chemotherapy-induced vomiting.
•Benzodiazepines like lorazepam reduce anticipatory nausea and vomiting. Miscellaneous therapies
with benefit in chemotherapy-induced emesis include cannabinoids, olanzapine, and alternative
therapies like ginger.
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53. SELECTED CLINICAL SETTINGS
•. Most antiemetic regimens produce greater reductions in vomiting than nausea.
•Clinicians should exercise caution in managing pregnant patients with nausea.
• Antihistamines like meclizine and doxylamine, antidopaminergics like prochlorperazine, and antiserotonergics like ondansetron
demonstrate limited efficacy.
• Some obstetricians offer alternative therapies including pyridoxine, acupressure, or ginger.
•Managing cyclic vomiting syndrome is challenging. Prophylaxis with tricyclic antidepressants, cyproheptadine, or β-adrenoceptor
antagonists can reduce the severity and frequency of attacks.
•Intravenous 5-HT3antagonists combined with the sedating effects of a benzodiazepine like lorazepam are a mainstay for treating acute
flares.
• Small studies report benefits with antimigraine agents, including the 5-HT1agonist sumatriptan, and selected anticonvulsants like
topiramate, zonisamide, and levetiracetam.
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54. Complications of Vomiting
Nutritional
◦ adults: weight loss; kids: failure to gain
Cutaneous (petechia, purpura)
Orophayngeal (dental, sore throat)
Esophagitis/ esophageal hematoma
GE Junctional: M-W tears; rupture (Boorhaave’s)
Metabolic: electrolyte, acid-base, water
Renal: prerenal azotemia; ATN; hypokalemic nephropathy
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55. Post-emetic purpura
(“mask phenomenom)
Cutis, 1986
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56. Mallory-Weiss tear with clot
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57. Two tears: one at 7 o’clock opposite other
tear at 1 o’clock
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58. Esophageal hematoma secondary to
forceful emesis
Digestive Diseases and Sciences 26: 1019, 1981
Lumen
mass
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59. ELECTROLYTE AND ACID-BASE
DISORDERS DUE TO VOMITING
Metabolic alkalosis
retention of HCO3
- + volume-
contraction
Hypokalemia
renal K+ losses + GI K+ loss +  oral K+
intake
Hypochloremia
gastric chloride losses
Hyponatremia
free water retention due to volume
contraction
130 78 28
3 40 0.8
Pearl: Patients with uremia
or Addison’s disease may
have normal or even high
serum K+ despite vomiting
Typical SMA-6
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60. NADER AL-ASSADI

61. Vomiting with
abdominal pain with
fever
• GE,TB,meningitis.
• Splenic mesenteric
infarction
Vomiting with
abdominal pain –no
fever
• Pyloric
obestruciton(acidic)
• Post pyloric
obstruction(alkaline)
• Large bowel
obstruction (fecal bad
odour )
Vomiting no abdominal
pain with fever
• Any cause of increase
ICP.
• Meningitis
,encephalitis.
Vomiting no
abdominal pain –no
fever.
• Any thing cause
sever headache with
out fever.
• Eg :
embolus,truma,CVA
Associated symptoms
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62. Bloody vomiting
Coffee
Cholingiocharcinoma
Cancer of
stomach
Fresh
Varices cancer Erosion
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63. DD OF coffee ground with jaundice:
1- end stage of liver diseases
2-cancer of stomach
3- Cancer of esophagus
4- cholingiocarcinoma
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64. NADER AL-ASSADI

65. Alarm symptoms
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66. NADER AL-ASSADI

67. Do you also have diarrhea? Do others in your community
(family, day care, cruise ship, summer camp) also have
vomiting and diarrhea?
Viral gastroenteritis
Food-borne illness
Do you have any symptoms of pregnancy, such as late
menstrual period or breast swelling, tingling, or
tenderness?
Early pregnancy (LR+ 2.70)
FOCUSED QUESTION
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68. Are you pregnant (frst trimester)? Hyperemesis gravidarum
Are you pregnant (second or third trimester)? AFLP or HELLP syndrome
Does the room feel like it is moving? (vertigo) Labyrinthitis (see Chapter 6)
Have you been receiving chemotherapy for cancer? Post chemotherapy nausea and vomiting
Has your weight gone up and down (30–40 lb) this
past year? Do you always vomit into the toilet and
never on the floor or in public? Do you make yourself
vomit?
Eating disorder (see Chapter 15)
Do you vomit without retching? Do you rechew and/or
reswallow your vomitus?
Rumination syndrome; not true vomiting
Do you have a history of kidney disease or failure? Uremia
Do you have a history of peptic ulcer? Have you been
taking nonsteroidal anti-inflammatory drugs (NSAIDs) or
aspirin?
Peptic ulcer or gastric outlet obstruction
Do you feel full after eating just a small amount of food
(early satiety)?
Gastric malignancy, gastric outlet obstruction
Do you chew on your hair? Bezoar
Do you have a history of heart disease? Acute myocardial infarction, digoxin toxicity
Have you had previous abdominal surgery? Intestinal obstruction due to adhesions
Is anyone else who ate or drank the same thing also having
nausea and vomiting?
Food poisoning
Did the symptoms occur within a few hours after eating or
drinking something?
Food poisoning due to Staphylococcus aureus or
Bacillus cereus toxins
Did you eat raw shellfsh? Food poisoning due to Vibrio vulnifcus
Did you eat shellfsh, and do you have numbness and
tingling around your mouth?
Paralytic shellfsh poisoning (saxitoxin)
Did you eat home canned or preserved food? Do you have
trouble swallowing? Is your mouth dry? Is your vision
blurry?
Botulism8
Did you eat raw fsh? Anisakiasis
Did you drink liquids that were stored in a metal
container? Do you also have a metallic taste?
Heavy metal ingestion (zinc, copper, tin, iron,
cadmium)
Did the bumps in the car ride make your abdominal pain
worse?
Peritonitis
Do you have diabetes? Diabetic ketoacidosis or gastroparesis
Does the child’s ear hurt? Is the child rubbing or pulling
on the ear?
Acute otitis media LR+ 3 to 7.39 (see Chapter 17)
Did the child recently have the flu or a cold? Did the child
receive aspirin?
Reye’s syndrome
Is there a family history of early childhood death?
Inherited metabolic disorders (urea cycle disorders,
Wilson’s disease)
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69. FOCUSED QUESTION
• Epigastric abdominal pain radiating to the
back?
Pancreatitis
• Abdominal pain that worsens with jolting
movements?
Bowel perforation
Peritonitis
• Migraine headaches? Cyclic vomiting syndrome
• Vertigo? Labyrinthitis
Do you get sick:
• Only as a passenger in a vehicle?
Motion sickness/sea sickness/space
sickness
• Only during periods of stress? Psychogenic
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70. Summary
Nausea and vomiting are features of many GI and non-GI
diseases and disorders.
Regardless of its cause, treatment of nausea and vomiting
should initially focus on replacing volume and electrolyte
deficits. Later on, nutritional deficits must be addressed.
Regardless of its cause, nausea and vomiting can cause
several life-threatening GI and non-GI complications.
Elucidation of the cause is often possible, and treatment of
the underlying cause will usually be successful.
Effective symptomatic therapies for nausea and vomiting are
available when the cause is unclear or when the treatment
of the underlying cause takes time to work.
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71. Reference
harrison's 20th edition.
K Sembulingam - Essentials of Medical Physiology, 6th Edition.
The Patient History - An Evidence-Based Approach to Differential Diagnosis, 2nd Edition.
Emetrol Cherry (phosphorated carbohydrate solution) package insert. Sarasota, FL: Preferred
Pharmaceuticals, Inc; 2012.
Ondansetron (Zofran) 32 mg, single IV dose: updated safety communication—product removal
due to potential for serious cardiac risks. FDA. December 4, 2012.
www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/uc
m330772.htm. Accessed August 29, 2013.
Roden DM. Drug-induced prolongation of the QT interval. N Engl J Med. 2004;350:1013–1022.
Kallergis EM, Goudis CA, Simantirakis EN, et al. Mechanisms, risk factors, and management of
acquired long QT syndrome: a comprehensive review. ScientificWorldJournal.
2012;2012:212178.
Medscape. NADER AL-ASSADI

72. Thank you
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