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25 Cards in this Set

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Nausea
Nausea is the subjective feeling of the need to vomit. It includes an unpleasant sensation in the mouth and stomach and can be associated with
salivation, sweating, dizziness, and tachycardia.
Vomiting
Vomiting is the forceful expulsion of the stomach contents through the
mouth, but is preceded by the relaxation of the esophageal sphincter, contraction of the abdominal muscles, and temporary suspension of
breathing.
Emetic Response: Neurophysiology
The CNS, the peripheral nervous system, and the gastrointestinal (GI) tract
are all involved in initiating and coordinating the emetic response. In the
CNS, the emetic (vomiting) center receives incoming signals from other parts
of the brain and the GI tract and then coordinates the emetic response by
sending signals to the effector organs.
Emetic Center: Neuorphys
The emetic center is located in the medulla oblongata of the brain, near the
nucleus tractus solitarius (NTS). The emetic center is stimulated by neurotransmitters released from the chemoreceptor trigger zone (CTZ), the GI tract, the cerebral cortex, the limbic system, and the vestibular system.
Emetic Response: Neurotransmitters
The major neurotransmitter receptors associated with the emetic response include serotonin (5-HT3) receptors, substance P neurokinin (NK)1 receptors, and dopamine D2 receptors. Other receptors involved include corticosteroid, acetylcholine, histamine, cannabinoid, gabaminergic, and opiate receptors.
Many of these receptors are targets for antiemetic therapy.
Emetic Response: CTZ
Chemoreceptor trigger zone (CTZ) is located in the area postrema on the floor of the fourth
ventricle in the brainstem; it lies outside the blood–brain barrier. When the
CTZ senses toxins and noxious substances in the blood and cerebrospinal fluid, it triggers the emetic response by releasing neurotransmitters that travel to the emetic center and the NTS. The major neurotransmitter receptors involved in this pathway include serotonin, dopamine, and
neurokinin-1.
Emetic Response: GI System
The GI system also plays a large part in the initiation of the emetic response. The GI tract contains enterochromaffin cells in the GI mucosa. When these cells are damaged by chemotherapy, radiation, or mechanical irritation, serotonin is released, which can stimulate the vagal afferents as well as directly stimulate the emetic center and NTS. The vomiting center then propagates the emetic response.
Emetic Response: Cerebral Ctx
The cerebral cortex and limbic system can stimulate the emetic center in response to emotional states such as anxiety, pain, and conditioned responses (anticipatory nausea and vomiting). Disorders of the vestibular system, such as vertigo and motion sickness, stimulate the emetic center through acetylcholine and histamine release.
Causes of nausea and vomiting (5)
1. Central nervous system (CNS) causes include increased intracranial pressure, migraine, brain metastases, vestibular dysfunction, alcohol intoxication, and anxiety.
2. Infectious disease causes include viral gastroenteritis, food poisoning, peritonitis, meningitis, and urinary tract infections.
3. Metabolic causes include hypercalcemia, uremia, hyperglycemia, and hyponatremia.
4. Gastrointestinal disorders, such as gastroparesis, bowel obstruction, distention, and mechanical irritation, can cause nausea and vomiting.
5. Among the many medications that can cause nausea and vomiting are cancer chemotherapy, antibiotics, antifungals, and opiate analgesics.
5-HT3 receptor antagonists
1. Mechanism of action
Granisetron and ondansetron competitively block 5-HT3 receptors located on the NTS, CTZ, and visceral afferent nerves. Thus, these drugs can prevent both peripheral and central stimulation of the vomiting center.
5-HT3 receptor antagonists---Administration and elimination
Granisetron and ondansetron
Oral and IV administration are equally effective; the drugs are metabolized in the liver
5-HT3 receptor antagonists---Adverse Effects
Headache, constipation
Substance P/NK1 Antagonist
1. Mechanism of action
Aprepitant is a competitive antagonist of substance P at NK1 receptors located in the CTZ and NTS.
Substance P/NK1 Antagonist--admin and elim
Aprepitant
Oral; metabolized in the liver
Substance P/NK1 Antagonist---Adverse Effects
Aprepitant
Fatigue, hiccups, headache, and diarrhea
Substance P/NK1 Antagonist--Drug interactions
Aprepitant
a. Corticosteroids
Aprepitant decreases the clearance of dexamethasone such that the dexamethasone dose (when used as an antiemetic) should be reduced.
b. Warfarin
Warfarin metabolism is induced such that its clearance is increased. The dose may need to be adjusted based on the patient’s coagulation status (INR).
c. Anticancer drugs
Several chemotherapy agents (e.g., etoposide, ifosfamide, vinca alkaloids, and others) are metabolized by the CYP3A4 enzyme system and the metabolism of these agents may be altered by aprepitant.
Corticosteroids
1. Mechanism of action
Dexamethasone
The mechanism of action of corticosteroids as antiemetics has not been determined. Corticosteroids may decrease serotonin release, antagonize
serotonin receptors, or activate corticosteroid receptors in the NTS.
Corticosteroids--admin and elim
Dexamethasone is available in both IV and oral formulations; metabolized in the liver
Corticosteroids--Adverse Effects
Dexamethasone
a. Insomnia, jitteriness, increased appetite, and GI distress.
b. Hyperglycemia can occur, especially in patients with pre-existing diabetes. These patients should monitor their glucose levels.
Metoclopramide
Metoclopramide provides antiemetic effects by blocking the dopaminergic receptors centrally in the CTZ. Peripherally, metoclopramide increases lower esophageal sphincter tone, aids gastric emptying, and accelerates transit through the small bowel, possibly through the release of acetylcholine. Side
effects include sedation and extrapyramidal side effects, such as dystonia
and akathesia.
Prochlorperazine
Phenothiazines such as prochlorperazine block dopamine receptors in the CTZ. As with metoclopramide, side effects include sedation and extrapyramidal side effects.
Nabilone
Cannabinoids have long been used for refractory nausea and vomiting. This is based on the effect of the CNS cannabinoid receptors on the CTZ, the NTS, and the emetic center. Nabilone, an oral cannabinoid, is associated with side effects, such as drowsiness, dry mouth, dysphoria, vertigo, and euphoria.
Olanzapine
Olanzapine is an atypical antipsychotic agent that antagonizes several serotonin and dopamine receptors as well as other neurotransmitter receptors. The common side effects of olanzapine include sleepiness, dry
mouth, and dizziness.
Scopolamine
Motion sickness may be associated with nausea and vomiting. Anticholinergic agents and antihistamines that cross,the blood–brain barrier effectively prevent and treat motion sickness. Scopolamine is a muscarinic,receptor antagonist that can prevent motion sickness. It is available as a topical patch, which bypasses the problem of GI symptoms associated with motion sickness.
Summary of use of antiemetics in treating nausea and vomiting