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Boards: GI > Gastrointestinal Drugs > Flashcards

Gastrointestinal Drugs Flashcards

1
Q

Examples - Antiemetic Drugs

A
  1. maropitant
  2. ondansetron
  3. metoclopramide
  4. promazine derivatives (ACP, CPZ)
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2
Q

NEUROKININ-1 RECEPTOR ANTAGONISTS

A

-Ex: maropitant

MOA: Blocks action of substance P in CNS and at peripheral NK-1 receptors in GI tract

Peripheral, Central Effects

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3
Q

Other Effects of NK1 R antagonists

A

Bone marrow hypoplasia in puppies younger than 11 weeks old

Other effects beyond antiemesis: Anti-inflammatory, Neuroprotectant, hepatoprotectant, MAC reduction/ visceral analgesia, anti-tumor

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4
Q

5-HT3 R Antagonists

A

Ex: ondansetron

MOA: Competitive serotonin receptor antagonists (peripheral in intestines if PO and centrally within CRTZ and medullary vomiting center if injected)

Peripheral, Central Effects

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5
Q

5-HT3 R Antagonist - metabolism

A

Metabolized by liver P-450 enzymes, then eliminated in urine and bile

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6
Q

5-HT3 R Antagonists - AEs

A

Adverse effects: Minimal; May cause in humans constipation/ diarrhea/ somnolence/ prolonged QT interval; May decrease efficacy of tramadol

Potential for Serotonin Syndrome

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7
Q

Metoclopramide

A

Antiemetic MOA: Dopamine antagonist + Serotonin receptor antagonist (5-HT3 antag.)

Prokinetic MOA: Dopamine antagonist +/- Increased sensitivity of SI smooth mm to ACh

Cats are thought to have a paucity of dopamine receptors – this is why it seems less effective

Central emetogens, peripheral and central for pro kinetic activity

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8
Q

Effects of Metoclopramide

A

Blocks CRTZ: antiemetic at 1-2 mg/kg q24h

Gastric prokinetic activity to facilitate gastric emptying and decreases GER requires higher doses like LD 0.4mg/kg followed by 0.3 mg/kg/h

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9
Q

Metoclopramide Excretion

A

Excreted by kidneys so use care in patients with substantially decreased GFR&raquo_space; Renal dysfunction allows for high blood levels&raquo_space; Extrapyramidal signs with hyperactivity/ frenzied behavior

Also risk of serotonin syndrome

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10
Q

Promazine Derivatives: ACP, CPZ

A

MOA: Antidopaminergic (D2) + Antihistamine effects that block the CRTZ and at higher doses also the medullary vomiting center

CENTRAL EFFECTS

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11
Q

Effects of Promazine Derivatives

A

Also alpha blockers but antiemetic effects are typically achieved at doses lower than those needed to produce sedation and hypotension

Can produce brady- or tachy-cardia but are antiarrhythmic;

May potentiate extrapyramidal effects of metoclopramide (so use caution and maybe don’t use both together)
Risk of serotonin syndrome

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12
Q

Prokinetic Drugs

A
  1. 5-HT4 R Agonists
  2. Cholinomimetic Drugs
  3. Motilin R Agonists
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13
Q

Gastric Protectants

A
  1. H2 R Antagonists
  2. PPIs
  3. Sucralfate
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14
Q

5-HT4 SEROTONERGIC AGONISTS (EX-CISAPRIDE)

A

Most effective class of prokinetic drugs in vet med (more effective than metoclopramide at treating GER and delayed gastric emptying)

Uses: Treat GER, poor gastric emptying, and chronic constipation; Increases gastroesophageal sphincter pressure; Increases SI motility

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15
Q

Limitations of 5-HT4 R Agonists

A

Does NOT work on striated muscle, so will not enhance esophageal motility in megaesophagus and in fact may make regurg worse in those patients because it increase LES tone

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16
Q

Cholinomimetic Drugs

A

Ex: ranitidine, bethanechol

17
Q

Ranitidine MOA

A

Inhibits acetylcholinesterase&raquo_space; Promote gastric emptying (minimal colonic motility)

Also H2 R antagonism

18
Q

Anticholinergics

A

–Scopalamine (effective for motion sickness in people, less so in vet med), atropine
–Block M1 R - vomiting caused by vestibular stimulation, stimulation of CTRZ

Not practical for many causes of vomiting in vet med, significant SE

Scopolamine: excitement in many animals, esp cats

19
Q

Glucocorticoids (steroids)

A

Block PGE2 production

20
Q

Motilin R Agonists

A

MOA: Stims motilin receptors&raquo_space; Promotes SI and LI peristalsis + Increases LES pressure

Erythromycin only

Other macrolides have different carbon structure, unable to bind to motion R

PERIPHERAL EFFECT

21
Q

Misoprostol

A

Prostaglandin E analog&raquo_space; Enhances colonic motility to treat patients with nonresponsive constipation

Stims secretion of mucus and bicarb

Increases gastric mucosal BF

Acts directly on parietal cells to inhibit acid secretion

PERIPHERAL EFFECTS

22
Q

Adverse Effects of misoprostol

A

Diarrhea; Uterine contraction which can cause abortion

23
Q

Gastroprotectants - Usage

A

typically indicated to heal existing gastric ulcers but are not effective at preventing ulceration when the cause still exists.

While drugs that decrease gastric acid secretion are NOT antiemetic (eg have no effect on CRTZ or MVC), can lessen nausea with an antidyspeptic effect

24
Q

Causes of GI Ulceration

A

Gastric hypoxia and hypoperfusion (d/t hypotensive shock, SIRS, severe life-threatening illness) with or without steroids or NSAID use

Hyperacidity from gastrinoma or MCT may cause gastric ulcers but more commonly duodenal

Liver failure / FB may also cause gastric ulcers

25
Q

NSAID GI Ulceration - locations in horses

A

stomach, RDC - anywhere

26
Q

NSAID GI Ulceration - location in camelids

A

third compartment

27
Q

NSAID GI Ulceration - dogs

A

antrum, proximal duodenum

28
Q

NSAID GI Ulceration - ruminants

A

Abomasum

29
Q

HISTAMINE-2 RECEPTOR ANTAGONISTS (H2RAS) EX- FAMOTIDINE, CIMETIDINE

A

MOA: Block histamine receptor on gastric parietal cell to competitively inhibit gastric acid secretion (vs PPIs which are noncompetitive) –> more effective at decreasing gastric acid secretion

Onset of action is almost immediate

30
Q

HISTAMINE-2 RECEPTOR ANTAGONISTS (H2RAS) EX- FAMOTIDINE, CIMETIDINE Metabolism

A

First pass hepatic metabolism with PO admin; cimetidine/ ranitidine metabolized by liver but famotidine excreted almost completely unchanged in urine

Cimetidine: CYP450 inhibition

31
Q

Cimetidine’s Effects on Hepatic CYP450

A

Markedly inhibits hepatic P450 enzymes:

decreases metabolism of lidocaine/ theophylline/ metronidazole/ etc&raquo_space; Toxicity (famotidine barely affects this at all)

Cimetidine also decreases hepatic BF by about 20%

Cimetidine is associated with more AE, uncommon with ranitidine or famotidine

32
Q

PPIs: omeprazole, pantoprazole

A

Somewhat effective as prophylactic against NSAID-induced GUE (gastric ulceration and erosion), but not completely effective

MOA: Irreversibly inhibit H-K ATPase on luminal side of parietal cell&raquo_space; Stops secretion of H+ ions into gastric lumen

Non-competitive inhibition

33
Q

PPI Onset of Action

A

2-5 days before maximal acid suppression occurs, but the immediate effects may still be superior to those of famotidine, and suppression of acid continues for a few days after admin d/t irreversible inhibition of the proton pump enzyme

Can decrease GER during GA but will not prevent it

34
Q

AEs PPIs

A

Diarrhea; Inhibit P-450 enzymes (omep&raquo_space; pantop)

35
Q

Sucralfate

A

Aluminum hydroxide compound that binds to epithelial cells in the acidic environment of stomach

Physical barrier to ulcer to protect ulcer from acids

Stims local production of prostaglandins, binding to epidermal growth factor (to encourage mucosal repair)

Boards: GI (4 decks)

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