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MANAGEMENT OF
CHEMOTHERAPY INDUCED
NAUSEAAND VOMITING
LECTURE BY
APOLLOJAMES, M.Pharm.,(Pharm.Prac)
Associate professor,
Dept. of Pharmacy practice,
Nandha college of Pharmacy, Erode, Tamilnadu.
Nausea and vomiting in the person with cancer
can be caused by many different things such as
• Chemotherapy
• Radiation therapy
• Cancer itself, if it is in brain
• Bowel slow down (paresis) or blockage or even constipation.
• Inner ear problem (two vestibular nerves in your inner ear send
information about head movement, when these nerve inflamed,
cause labyrinthitis)
• An imbalance of minerals and salts
• Infections
• Anxiety
• Expectation of vomiting due to past vomiting in the same
setting (anticipatory vomiting). These triggers vomiting centre in
the brain, certain areas of esophagus, stomach, small intestine
and large intestine are triggered.
CLASSIFICATION OF N / V
• ACUTE- Nausea and vomiting during the first 24 hours
period immediately after chemotherapy administration.
• DELAYED- Nausea and vomiting more than 24 hrs after
chemotherapy and may continue for upto 6 or 7 days after
chemotherapy.
• ANTICIPATORY: Nausea and vomiting before patients
receive their next chemotherapy treatment, conditioned
response.
• BREAK THROUGH: Nausea and vomiting, despite
standard anti-emetic therapy (prophylactic therapy), which
require additional (rescue therapy).
• REFRACTORY: patient who have failed on both standard
and rescue medication.
EMETOGENIC POTENTIAL OF
CANCER CHEMOTHERAPY AGENTS:
• LEVEL 1: Very low emetic risk
• LEVEL 2: low emetic risk
• LEVEL 3: moderately emetogenic
• LEVEL 4: highly emetogenic
• LEVEL 5: very highly emetogenic.
MANAGEMENT:
• Aprepitant (NK1 receptor antagonist)
• Dolasetron (5HT3 receptor antagonist)
• Granisetron (5HT3 receptor antagonist)
• Ondansetron (5HT3 receptor antagonist)
• Palonosetron (5HT3 receptor antagonist)
• Proclorperazine (D2 receptor antagonist)
• Promethazine (strong antagonist of H1 receptor,
moderate affinity for 5-HT2, D2)
• Lorazepam
MANAGEMENT:
• Metoclopramide (dopamine receptor antagonist)
• Dexamethasone (crosses cell membrane and binds with
high affinity to specific cytoplasmic receptors, inhibits
leukocyte infiltration in the site of inflammation, decrease
inflammatory response, suppression and humoral immune
response. The anti-inflammatory action of
dexamethasone are thought to involve phospholipase A2
inhibitory protein, lipocortin, which control the biosynthesis
of potent mediators of inflammation such as PG’S and
leukotriene).
• Famotidine (H2 receptor antagonist)
• Ranitidine (H2 receptor antagonist)
THANK YOU

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Management of chemotherapy induced nausea and vomiting

  • 1. MANAGEMENT OF CHEMOTHERAPY INDUCED NAUSEAAND VOMITING LECTURE BY APOLLOJAMES, M.Pharm.,(Pharm.Prac) Associate professor, Dept. of Pharmacy practice, Nandha college of Pharmacy, Erode, Tamilnadu.
  • 2. Nausea and vomiting in the person with cancer can be caused by many different things such as • Chemotherapy • Radiation therapy • Cancer itself, if it is in brain • Bowel slow down (paresis) or blockage or even constipation. • Inner ear problem (two vestibular nerves in your inner ear send information about head movement, when these nerve inflamed, cause labyrinthitis) • An imbalance of minerals and salts • Infections • Anxiety • Expectation of vomiting due to past vomiting in the same setting (anticipatory vomiting). These triggers vomiting centre in the brain, certain areas of esophagus, stomach, small intestine and large intestine are triggered.
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  • 4. CLASSIFICATION OF N / V • ACUTE- Nausea and vomiting during the first 24 hours period immediately after chemotherapy administration. • DELAYED- Nausea and vomiting more than 24 hrs after chemotherapy and may continue for upto 6 or 7 days after chemotherapy. • ANTICIPATORY: Nausea and vomiting before patients receive their next chemotherapy treatment, conditioned response. • BREAK THROUGH: Nausea and vomiting, despite standard anti-emetic therapy (prophylactic therapy), which require additional (rescue therapy). • REFRACTORY: patient who have failed on both standard and rescue medication.
  • 5. EMETOGENIC POTENTIAL OF CANCER CHEMOTHERAPY AGENTS: • LEVEL 1: Very low emetic risk • LEVEL 2: low emetic risk • LEVEL 3: moderately emetogenic • LEVEL 4: highly emetogenic • LEVEL 5: very highly emetogenic.
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  • 8. MANAGEMENT: • Aprepitant (NK1 receptor antagonist) • Dolasetron (5HT3 receptor antagonist) • Granisetron (5HT3 receptor antagonist) • Ondansetron (5HT3 receptor antagonist) • Palonosetron (5HT3 receptor antagonist) • Proclorperazine (D2 receptor antagonist) • Promethazine (strong antagonist of H1 receptor, moderate affinity for 5-HT2, D2) • Lorazepam
  • 9. MANAGEMENT: • Metoclopramide (dopamine receptor antagonist) • Dexamethasone (crosses cell membrane and binds with high affinity to specific cytoplasmic receptors, inhibits leukocyte infiltration in the site of inflammation, decrease inflammatory response, suppression and humoral immune response. The anti-inflammatory action of dexamethasone are thought to involve phospholipase A2 inhibitory protein, lipocortin, which control the biosynthesis of potent mediators of inflammation such as PG’S and leukotriene). • Famotidine (H2 receptor antagonist) • Ranitidine (H2 receptor antagonist)