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GI Week 4 - WLB > Antiemetics and Treatments for IBD - Fitz > Flashcards

Antiemetics and Treatments for IBD - Fitz Flashcards

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1
Q

What are the three decontamination agents that we need to know?

A
  1. ACTIVATED CHARCOAL
  2. IPECAC
  3. POLYETHYLENE GLYCOL SOLUTION
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2
Q

What are the 7 classes of drugs that we need to know for antiemetics?

A
  1. 5HT3 antagonists
  2. Anticholinergics
  3. NK1 antagonists
  4. Cannabinoids
  5. H1 antagonists
  6. D2 antagonists
  7. Corticosteroids
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3
Q

What are the four antiemetic 5HT3 antagonists that we need to know?

A
  • Ondansetron
  • Dolasetron
  • Granisetron
  • Palonosetron
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4
Q

What is the one Anticholinergic drug that works as an antiemetic that we need to know?

A

Scopolamine

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5
Q

What is the one NK1 antagonist drug that acts as an antiemetic that we need to know?

A

APREPITANT / FOSAPREPITANT

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6
Q

What are the two Cannabinoid drugs that act as antiemetics that we need to know?

A

Dronabinol

and

Nabilone

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7
Q

What are the three H1 antagonist drugs that act as antiemetics that we need to know?

A
  • Dimenhydrinate
  • Diphenhydramine
  • Meclizine
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8
Q

What are the five D2 antagonists that act as antiemetics that we need to know?

A
  • Droperidol
  • Metoclopramide
  • Prochlorperzaine
  • Promethazine
  • Thiethylperazine
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9
Q

What are the two corticosteroids that act as antiemetics that we need to know?

A
  • Dexamethasone
  • Methylprednisolone
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10
Q

Why did the FDA has stopped OTC sales of the emetic agent IPECAC?

A

Administration of IPECAC is particularly dangerous if the suspected poison is corrosive, a petroleum distillate or a rapidly-acting convulsant.

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11
Q

What type of drugs are the only truly effective agents for ameliorating cancer chemotherapy-induced emesis (esp. caused by cisplatin)?

A

5HT3 antagonists (“-setrons”)

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12
Q

What is the most effective agent for the treatment of motion sickness when administered via a transdermal patch?

A

Scopolamine

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13
Q

What are the four important locations that need to be considered when thinking about the physiology behind vomiting and possible ways to treat/prevent vomiting?

A
  1. Sensory receptors:
    • in the stomach and small intestine, the pharynx and the inner ear
    • visual, olfactory and painful stimuli can also elicit vomiting
  2. Chemoreceptive trigger zone (CTZ):
    • located in the area postrema, on the floor of the 4th ventricle → OUTSIDE THE BLOOD BRAIN BARRIER
    • primary region responsible for detection of blood-borne emetics
  3. Vomiting centre
    • connected to the CTZ
    • responsible for the initiation and coordination of the complex motor patterns needed for vomiting
  4. “Higher centres”
    • responsible for vomiting due to memory, fear, dread and anticipation
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14
Q

What are the 3 types of pathways that activate the vomiting center?

A
  1. MECHANICAL AND/OR PAINFUL STIMULI especially those from:
    • INNER EAR (motion, antibiotics) → cerebellum → vomiting centre
    • LOCAL GI IRRITATION (cytotoxic drugs, bacteria, radiation): vagal and sympathetic afferents from the stomach and small intestine that can be modulated by the action of 5HT3 receptors → solitary tract nucleus AND the chemoreceptive trigger zone → vomiting centre
    • PHARYNX (gag reflex): glossopharyngeal and trigeminal afferents → solitary tract nucleus → vomiting centre
  2. BLOOD BORNE EMETICS → chemoreceptive trigger zone → vomiting centre
  3. “HIGHER CENTERS”: project directly to the vomiting centre via ill-defined routes (anticipatory nausea)
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15
Q

What is the MOA of IPECAC?

A

local GI irritant effect as well as acting on CTZ

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16
Q

Are antiemetics generally more effective at preventing vomiting or stopping emesis once its started?

A

Preventing vomiting

17
Q

What is the MOA of DOLASETRON, GRANISETRON, ONDANSETRON, and PALONOSETRON?

A
  • blockade of peripheral 5HT3 receptors on intestinal vagal afferents
    • prevent vomiting related to significant vagal stimulation
  • CNS actions at both the CTZ and vomiting center
18
Q

What is the MOA of Scopolamine?

A
  • inhibition of muscarinic receptors in the cerebellum
  • rapidly and fully distributed in the CNS
    • particularly effective in the prevention of motion sickness
19
Q

What antiemetic(s) inhibit the neurotransmitter Substance P from binding to NK1 tachykinin receptors in both the CNS and GI tract preventing the stimulation of nausea and vomiting?

A

Aprepitant / Fosaprepitant

20
Q

What antiemetics are used for the prevention of acute and delayed phase of chemotherapy-induced nausea and vomiting?

A

Aprepitant / Fosaprepitant

21
Q

What three antiemetics prevent nausea/vomiting by causing sedation and possibly having some antimuscarinic activity?

A
  • H1 antagonists
    • Diphenhydramine
    • Meclizine
    • Dimenhydrinate
22
Q

What antiemetics act through inhibition of dopaminergic (D2) and muscarinic receptors in the CTZ?

A
  • D2 receptor antagonists:
    • Droperidol
    • Metoclopramide
    • Prochlorperzaine
    • Promethazine
    • Thiethylperazine
23
Q

What antiemetic drugs have side effects that include euphoria, dysphoria, sedation, hallucinations, dry mouth and increased appetite (may benefit cancer patients); and occasionally cause tachycardia, conjunctival injection and orthostatic hypotension?

A
  • Cannabinoids:
    • Dronabinol
    • Nabilone

(MOA not understood → act on central cannabinoid receptors)

24
Q

Which antiemetic drugs have an unknown mechanism of action (with respect to antiemetic effects) but are known to act on receptors that are widespread in the brain including the nucleus of the solitary tract, the hypothalamus and the cortex, which are all regions with inputs to the vomiting center?

A
  • Corticosteroids:
    • Methylprednisolone
    • Dexamethasone
25
Q

What are the four anti-inflammatory drugs used in the treatment of IBD that we need to know?

A
  1. Mesalamine (5-ASA)
  2. Balsalazide
  3. Osalazine
  4. Sulfasalazine
26
Q

What are the six immunosuppressant drugs used in the treatment of IBD that we need to know?

A
  • Corticosteroids:
    • Budesonide
    • Prednisone
    • Prednisolone
  • Anti-Metabolites:
    • Azathioprine
    • 6-Mercaptopurine
    • Methotrexate
27
Q

What is the one Anti-TNFalpha drug used in the treatment of IBD that we need to know?

A

Infliximab (Remicade)

28
Q

What are the NSAIDs and corticosteroids used in the treatment of chronic inflammatory bowel disease designed to do?

A

have local actions within the large intestine in order to limit systemic side effects

29
Q

What drug used to treat IBD can lead to symptomatic improvement and remission in patients with moderately severe Crohn’s disease, and has side effects similar to those described for other monoclonal antibodies (infections, infusion reactions)?

A

Infliximab

30
Q

What IBD treatments are used to treat mild disease states?

A

BUDESONIDE
Topical CORTICOSTERIODS
Antibiotics
5-ASA COMPOUNDS

31
Q

What IBD treatments are used to treat moderate disease states?

A

TNF ANTAGONISTS
Oral CORTICOSTERIODS
METHOTREXATE
AZATHIOPRINE / 6-MERCAPTOPURINE

32
Q

What IBD treatments are used to treat severe disease states?

A

Surgery
TNF ANTAGONISTS
IV CORTICOSTEROIDS

33
Q

What are the various sites of action for the 5-ASA IBD treatments?

A
  • Small intestines + Colon
    • Mesalamine
  • Colon
    • Balsalazide
    • Sulfasalazide
34
Q

Why is Budesonide a good immunosuppressive agent, particularly for use in mild to moderate Crohn’s disease involving the ileum and proximal colon?

A

BUDESONIDE is subject to extensive, rapid first pass metabolism (low oral bioavailability) → local (GI) rather than systemic effect compared to conventional steroids when given in a controlled-release oral formulation

35
Q

What is the MOA of Infliximab?

A

antibodies that bind to both soluble and receptor-bound TNFα → preventing binding of the cytokine to its receptors

chimeric (~95% human)

GI Week 4 - WLB (8 decks)

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