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3. Clin Pharm > GI drugs 1 > Flashcards

GI drugs 1 Flashcards

1
Q

Anti-emetic drugs use

A
  • used to non-specifically manage vomiting induced by:
  • drugs and other foreign chemicals
  • radiation therapy sickness or motion sickness (prophylaxis, therapy)
  • organ dysfunction
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2
Q

how are antiemetics classified

A

by the receptor they exert their dominant effects on
> however considerable overlap exists

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3
Q

where is the emetic center in the brain

A

medulla

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4
Q

what general categories of locations in the body do antiemetics work on

A
  • labrynths
  • higher centers
  • chemoreceptor trigger zone
  • peripheral organs
  • emetic center (medulla)
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5
Q

important anti-emetic categories for our use

A
  • anti-histamines
  • dopamine antagonists
  • serotonin
  • neurokinin -1 antagonists
  • other agents
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6
Q

anti-histamines that are used as antiemetics

A
  • diphenhydramine (Benadryl®)
  • meclizine (Bonamine®)
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7
Q

what kind of emesis do anti-hostamines work to stop? what is a common side effect? what other properties do these drugs have?

A
  • can be used to control motion sickness
  • sedation can be common side-effect with the H1 blockers; paradoxical excitement in cats possible
  • many have anticholinergic properties as well
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8
Q

types of dopamine antagonists that are used as anti-emetics

A
  • phenothiazines
    > prochlorperazine (Stemetil®), acepromazine (Ace®)
  • metoclopramide (Maxeran®)
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9
Q

how do phenothiazines work as anti-emetics? mechanism of action?

A
  • these are broad-spectrum anti-emetics as they are capable of blocking several neurotransmitters
  • principal mechanism of actions is blockade of dopamine receptors in the CTZ
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10
Q

phenothiazines adverse effects

A
  • sedation
  • hypotension from α-adrenergic blockade
  • can lower seizure threshold in epileptics
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11
Q

how does metoclopramide work as an anti-emetic? what type of emesis is it useful for?

A
  • effectively blocks emesis mediated at the CTZ
    > antagonizes dopamine (low doses)
    > antagonizes serotonin (5-HT3) (higher doses)
  • also has peripheral antiemetic effects thru prokinetic effects promoting upper GI motility
    > contraindicated in GI obstruction or perforation
  • useful for emesis induced by GI disease and possibly chemotherapy
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12
Q

adverse effect of metoclopramide

A

CNS stimulation is possible adverse effect

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13
Q

types of serotonin antagonists used as anti-emetics

A
  • Ondansetron (Zofran®)
  • Granisetron (Kytril®)
  • Mirtazapine (Remeron®)
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14
Q

how do Serotonin (5-HT3) antagonists work as anti-emetics? what kind of vomitng are they useful for? are they well tolerated?

A
  • block central (CTZ) and peripheral 5-HT3 receptors
  • useful for refractory vomiting
    v chemotherapy
    v parvovirus infection
    v post-operative vomiting
    v pancreatitis
  • generally very well tolerated
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15
Q

how does Mirtazapine work as an antiemetic? when can it be useful?

A
  • Antidepressant in humans
  • Antiemetic effects in cats; also appetite stimulation
    > Maybe useful in vomiting with chronic kidney disease
    > Attributed to 5-HT3 receptor antagonism
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16
Q

Neurokinin -1 antagonist used as an anti-emetic

A

Maropitant

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17
Q

how do neurokinin -1 antagonists work as anti-emetics? when are they useful?

A
  • block effects of substance P in the emetic center
  • licensed for use in dogs and cats
    > acute vomiting from parvovirus, gastroenteritis and pancreatitis
    > prevention of chemotherapy-induced vomiting
    > motion sickness
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18
Q

what form are neurkinin -1 antagonists available in

A

available in injectable (SC or IV) and tablets

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19
Q

Neurokinin -1 antagonists adverse effects

A
  • swelling/pain at injection site possible
  • some vomiting and hypersalivation possible with tabs
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20
Q

Maropitant may be useful for what conditions, other than as an antiemetic

A

interest with maropitant for analgesia and pain

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21
Q

glucocorticoid used as an anti-emetic

A

Dexamethasone

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22
Q

glucocorticoids use as anti-emetic - when is it used? how does it work? is it indicated?

A
  • Veterinary approved injectable; but not indicated for tx of vomiting
  • May work to reduce vomiting by inhibiting prostaglandin production
  • Can be added to other antiemetics for refractory vomiting
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23
Q

Cannabinoids use as anti-emetic? can veterinarians dispense it?

A

Cannabidiol (CBD)
- Potential for antiemetic effects based on human experience with
antineoplastic drugs; works by activating CB1 receptors in the CNS
- Cannabis Act does not include veterinary patients
> Currently, no legal way for veterinarians to prescribe, dispense or recommend medical marijuana or CBD to veterinary patients in Canada

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24
Q

why induce emesis?

A

Emesis is induced pharmacologically to empty anterior part of the GI tract
- prior to general anesthesia
- following ingestion of non-corrosive intoxicants

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25
Q

types of emetics

A
  1. Peripherally acting (reflex) emetics
  2. Centrally acting emetics
26
Q

types of Peripherally acting (reflex) emetics

A
  • “household remedies”
    > table salt with/without warm water
    > hydrogen peroxide (3%)
  • Ipecac syrup—contains alkaloid “emetine”
27
Q

hydrogen peroxide emesis adverse consequence

A

aspiration of foam possible

28
Q

ipecac syrup contains what? adverse effect and how to deal with it? 2nd mechanism of action aside from reflex emesis?

A
  • contains alkaloid “emetine”
  • cardiotoxicity possible with repeat doses
    > gastric lavage to remove if no vomiting
  • can also activate CTZ centrally
29
Q

Centrally acting emetics

A
  • Apomorphine
  • α2-agonists eg Xylazine,
    dexmedetomidine
30
Q

when can apomorphine be used for emesis? when shouldn’t it be? how does it work?

A

Apomorphine—derivative of morphine
- used in dogs successfully
- use in cats controversial; less successful
- stimulates CTZ via dopaminergic receptors

31
Q

forms that apomorphine comes in? how fast it works?

A
  • tablets or injectable (SC or conjunctival)
  • emesis usually in 2-10 minutes
32
Q

is repeat dosing of apomorphine effective? why? adverse effects?

A
  • repeat dosing less effective; direct depression the vomiting center
  • respiratory depression possible with excess dosing; protracted vomiting also possible
33
Q

α2-agonists - when are they used as emetics? mechnaism of action?

A
  • more reliable in cats
  • activates CTZ
34
Q

requisite for GI ulceration

A

Acid injury of the gastroduodenal mucosa

35
Q

Defense mechanisms that oppose gastric acid injury

A

v mucus (alkaline) production
v bicarbonate secretion into lumen
v mucosal re-epithelialization and repair of gastric barrier
v mucosal blood flow
v local PGE2 production—cytoprotection

36
Q

Factors predisposing ulcer formation include:

A

v Diet; composition and feeding practices
v NSAIDs and corticosteroids
v Stress; transport
v Exercise intensity (horses)
v Disruption of mucosal blood supply

37
Q

gastric acid secreted by what? 3 sources of input required to yield HCl production?

A

secreted by parietal cells of the fundic region of the glandular stomach

3 sources of input:
v ACh (vagus and enteric cholinergic ganglion cells)
v Histamine (enterochromaffin-like cells)
v Gastrin (circulating hormone from gastric G-cells)

38
Q

targets of pharmalogical intervention to reduce or inhibit HCl production, as anti-ulcer agents

A
  1. binding of histamine to H2 receptors on perietal cells
  2. ATPase
  3. parietal cell apical surface
  4. acid secretion
  5. PGE2 binding to parietal cells
39
Q

ANTI-ULCER AGENTS broad categories based on functionality

A

-Gastric Antisecretory Drugs
-Mucosal Protectants

40
Q

types of gastric antisecretory drugs

A
  1. H2 Blockers
  2. Proton Pump Inhibitors
41
Q

types of H2 blockers

A
  • Cimetidine (Tagamet®)…used less now !
  • Ranitidine (Zantac®)
  • Famotidine (Pepcid®)
42
Q

mechanism of action of H2 blockers

A

Histamine binds to H2 receptors on parietal cells to cAMP and proton pump activity
- histamine is the common mediator of HCl secretion
- H2 blockers competitively inhibit histamine binding
- H2 blockers reduce HCl acid production including gastric juice and pepsin
content of secretions

43
Q

Drug interactions of H2 blockers

A

altered gastric pH—affect absorption of other drugs requiring an acid environment

44
Q

Indications for H2 blockers? is there good evidence?

A

evidence lacking !!
v Gastric and duodenal erosions and ulcers
v Uremic and stress-related gastritis
v Hypersecretory conditions (gastrinoma)
v Duodenal gastric reflux and esophageal reflux
v NSAID-induced ulcers

45
Q

Cimetidine - how it works and what is its use? adverse effects?

A

H2 blocker
v Potent inhibitor of P450 metabolizing enzymes and drug interactions possible !!
v Ability to raise stomach pH in dogs questionable; efficacy in horses ?
v Rebound hypersecretion possible upon stopping drug; consider tapering off
drug

46
Q

Rantidine - how it works and how it compares to cimetidine?

A

H2 blovker
v More potent (4-10X) than cimetidine
v Rebound hypersecretion possible
v Minimal inhibition of P450 enzymes

47
Q

Famotidine - how it works and how it compares to ranitidine and cimetidine?

A

H2 blocker
v More potent (9X) than ranitidine and cimetidine (~30X) v Longest duration of action
v Less rebound hypersecretion
v Does not inhibit P450 enzymes

48
Q

Proton Pump Inhibitor we use

A

Omeprazole

49
Q

how do proton pump inhibitors work? are they good at what they do?

A

v Works by irreversibly binding the parietal cell H+/K+-ATPase (proton pump) which is the final step in gastric acid secretion
v Proton pump inhibitors are the most potent gastric antisecretory drugs available

50
Q

Omeprazole available in what form? when indicated? how long does it take to work?

A
  • Available as oral paste for horses (Gastrogard®)
  • Indicated for the treatment and prevention of ulcers in horses and
    foals
  • Also available in human approved tablets and capsules used in dogs and cats (Losec®)
  • May take 2-4 days to accumulate in parietal cells and produce a clinical effect
51
Q

-Mucosal Protectants, what types do we use

A
  • Sucralfate
  • Antacids
  • Misoprostol
52
Q

what is sucralfate and how does it work? when to use and what does it require to work? other useful properties?

A
  • Mucosal protectant
  • An orally administered disaccharide (sucrose) aluminum hydroxide product
    v Binds to and protects the ulcerated area (crater) from further damage by acid.
    > beneficial for tx of uclers, but not prevention
    v Requires an acid environment for activation
    v Tablets must be disintegrated for effects; crush or give as a liquid v Will also bind bile and pepsin reducing their harmful effects
    v May also increase local blood flow and beneficial
    prostaglandin production
53
Q

how do antacids work? possible adverse effects? formulations? possible other effects?

A
  • Antacids chemically neutralize HCl present in the gastric lumen thereby increasing gastric pH
    > Drug interactions possible from altered pH in the stomach, and also
    direct binding of other drugs eg fluorquinolones
  • Formulated as hydroxide bases of aluminum, magnesium and calcium
    > Aluminum containing agents may also stimulate prostaglandin production
54
Q

what is Misoprostol? how does it work? when is it used?

A
  • is a PGE analog
  • It is a mucosal protectant
    > Increases mucus production
    > Increases bicarbonate
    > Enhances re-epithelialization of mucosa
    > Increases local blood flow
  • It also has gastric antisecretory properties by reducing HCl production from parietal cells
  • Used for the prevention of gastric ulcers, especially involving NSAIDs; effectiveness in treating ulcers is less beneficial
55
Q

contraindication for misprostol and why

A

Contraindicated during pregnancy due to its promotion of uterine contractions

56
Q

how are GI motility disorders usually treated?

A

GI motility disorders are complex and poorly understood—treatment is often empiric

57
Q

what do prokinetics do? general mechanisms?

A

“Prokinetics” enhance the coordinated net
movement of ingesta thru the GI tract
v generally raise lower esophageal tone
v accelerate gastric emptying
v shorten intestinal transit time

58
Q

Indications for prokinetics:

A

v post-operative ileus
v delayed gastric emptying
v delayed intestinal transit
v megaesophagus, megacolon

59
Q

Prokinetics contraindicated:

A

v GI hemorrhage
v Obstruction
v Perforation

60
Q

regulation of GI motility can be divided into what?

A

Extrinsic
- vagus / pelvic nerves
> efferent activity to the GI tract
> acetylcholine released by these nerves act on receptors of intrinsic nerves, to stimulate motility and secretion
- sympathetic
> inhibitory for motility, but increase tone in GI tract sphincter

enteric / intrinsic
- ganglia and receptors on smooth muscle of GI tract
> control contractions mediated by acetylcholine, and relaxations mediated by NO2 or vasoactive intestinal peptide

61
Q

Drugs that promote the release of acetylcholine from terminals on the presynaptic neuron

A

??

3. Clin Pharm (11 decks)

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