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Introduction to Pharmacology > Gastrointestinal Drugs > Flashcards

Gastrointestinal Drugs Flashcards

1
Q

What are the 6 types of drugs used for treating gastrointestinal diseases?

A
  1. antiemetics
  2. drugs to treat diarrhea
  3. drugs to treat inflammatory intestinal diseases
  4. prokinetic drugs
  5. drugs to treat GI ulcers
  6. laxatives and cathartics
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2
Q

What neural plexuses are located in the walls of the gut? What is the ENS extensively innervated by?

A
  • SUBMUCOSAL PLEXUS: under the submucosa
  • MYENTERIC PLEXUS: between the inner circular muscle layer and the outer longitudinal muscle layer

nonadrenergic-noncholinergic (NANC) nerve fibers

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3
Q

ENS:

A
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4
Q

What is emesis? Where are all emetic signals coordinated? What supplies afferent input?

A

complex, protective, reflex activity with coordination centered in the brainstem

emetic center (vomiting center) in the mid brainstem

chemical trigger zone (CTZ), which is sensitive to drugs and toxins in the blood

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5
Q

What happens when emesis is pharmacologically induced? What are the 2 main purposes of pharmacologic emesis?

A

the anterior portion of the digestive tract is emptied

  1. preparation for induction of general anesthesia
  2. treatment of ingested, noncorrosive poisons
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6
Q

What are the 2 ways that substances induce emesis?

A
  1. distending the pharynx, esophagus, stomach, or duodenum (hollow organs)
  2. irritating the epithelium of the GI tract (gastric mucosa or pharynx)
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7
Q

What are 4 examples of peripherally acting (reflex) emetics?

A
  1. warm water/saline distends GI tract (can also dilute toxins)
  2. DOGS - oral administration of a solution of warm, saturated sodium chloride
  3. pharyngeal placement of a small amount of plain table salt or neutral salt crystals, such as sodium carbonate
  4. orally administered hydrogen peroxide (3%), copper sulfate (1%), or zinc sulfate (1%) —> careful of fatal aspiration pnemonia
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8
Q

What do prokinetic drugs do? What is a common instance they are used?

A

drugs that enhance the transit of intraluminal content and stimulate gastric emptying and rumen/intestinal motility

after surgery when intestinal motility is decreased, which can lead to ileus

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9
Q

What is Metoclopramide?

A

lipid-soluble derivative of para-aminobenzoic acid that acts as a central (antidopaminergic) and peripheral (antidopaminergic/cholinergic agonist) prokinetic drug

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10
Q

What are the 7 actions of Metoclopramide?

A
  1. D2 antagonist
  2. serotonin (5-HT3) antagonist
  3. serotonin (5-HT4) agonist
  4. increase the release of ACh in the GI tract
  5. increase gastric emptying
  6. increase the tone of the esophageal sphincter
  7. stimulate motility of the duodenum (less effective distally)
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11
Q

What endocrine effect does Metoclopramide have?

A

transient increase of prolactin and aldosterone

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12
Q

What are the 5 uses of Metoclopramide in small animals? When is use contraindicated?

A
  1. stimulate normal upper motility following corrected surgery
  2. volvulus
  3. postoperative ileus
  4. gastric ulceration
  5. idiopathic gastroparesis

GI obstruction or perforation

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13
Q

What are 2 uses of Metoclopramide in horses? What are 2 common undesirable side effects?

A
  1. reduce postoperative ileus
  2. stimulate small intestine (NOT large bowel)

behavioral changes and abdominal pain

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14
Q

Why is the use of Metoclopramide in ruminants less common? What can it be used successfully in? What side effect can occur in calves?

A

little usefulness in cattle - may increase rumen motility in cattle/sheep

cattle with functional pyloric stenosis

doses higher than 0.1 mg/Kg can cause severe neurological signs

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15
Q

Why was Cisapride removed from the market?

A

causes serious arrhythmias and death in people (not reported in animals)
- available via compounding pharmacists

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16
Q

What 3 effects does Cisapride have on ENS receptors? How does it effect the GI tract?

A
  1. 5-HT4 agonist on myenteric neurons
  2. 5-HT3 antagonist
  3. enhances ACh release at the myenteric plexus

ALL GI sites - esophagus, stomach, jejunum, ileum, small intestine, colon

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17
Q

What are the 4 major therapeutic uses of Cisapride?

A
  1. gastroesophageal reflux
  2. delayed gastric emptying
  3. small bowel motility disorders
  4. chronic constipation in cats (affects colonic smooth muscles)
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18
Q

How does Cisapride compare to Metoclopramide?

A
  • more effective for increasing lower esophageal sphincter tone in dogs
  • causes antegrade contraction along the whole GI tract
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19
Q

What is Domperidone? How does its mechanism of action compare to other drugs of the same class?

A

D2 antagonist that may also have α1-receptor antagonistic and serotonin (5-HT2) antagonist

mechanism of action and prokinetic effect is similar to metoclopramide
- accelerates small intestinal transit
- colonic activity unaffected

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20
Q

How has Domperidone been used in horses? What affect does the approved dose have?

A

treat fescue toxicity and agalactia
- forage-related disease involving endocrine disruptive effect of ergot alkaloids (from Neotyphodium coenophialum) on prolactin secretion

1.1 mg/Kg = oral absorption of 1-1.5% = no effect on GI function
- 5 mg/Kg = increased stomach emptying

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21
Q

How may Domperidone’s α2 antagonistic affects be used?

A

increases digital laminal microvascular flow, which may help treat laminitis

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22
Q

What is Erythromycin? How can it affect the GI tract?

A

macrolide antibiotic used to treat bacterial infections

at low doses (much lower than antibacterial dose), it stimulates GI motility

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23
Q

How does Erythromycin stimulate GI motility?

A

activated motilin receptors, allowing for motilin release from endocrine cells of the duodenal mucosa —> increases motor contraction
- most motilin receptors are on the stomach and proximal intestine

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24
Q

What is the main clinical use of Erythromycin? What are 2 major concerns?

A

increase gastric emptying and therapy of reflux esophagitis

  1. cause diarrhea by altering the normal bacterial flora of the intestine
  2. routine use can promote antibacterial resistance
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25
Q

Lidocaine is a well-known local anesthetic. How can it be used on the GI tract?

A

IV infusion of lidocaine improves intestinal motility in horses to reduce postoperative ileus

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26
Q

What are 3 common causes of postoperative ileus? What does this cause?

A
  1. sympathetic stimulation
  2. pain
  3. inflammation

inhibits smooth muscle motility in the intestine

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27
Q

How is Lidocaine thought to work as a prokinetic? What are 3 possible adverse effects? How can they be avoided?

A

not a direct prokinetic - may inhibit intestinal inflammation and reperfusion injury via suppression of painful stimuli

  1. muscle fasciculation
  2. ataxia
  3. seizures
    - decrease infusion rate
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28
Q

What 3 peripheral opiate antagonists can act as GI prokinetics? How do they work?

A

Alvimopan, Methylnaltrxone, Naloxegol

block the activation of µ-receptors on the submucosal plexus, myenteric plexus, and longitudinal muscle of the ileum, which would have decreased propulsive motility of intestinal smooth muscle

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29
Q

How do Alvimopan and Methylnaltrexone compare in potency and duration?

A

(peripheral opiate antagonists)

Alvimopan > Methylnaltrexone

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30
Q

How is Alvimopan administered? What does it do?

A

(peripheral opiate antagonist)
orally —> low bioavailability (6%)

produces a local effect on the intestine to promote motility

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31
Q

What is Naloxegol used for?

A

oral treatment of opioid-induced constipation

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32
Q

What are the 4 principal drugs used to manage GI ulceration in small and large animals?

A
  1. histamine (H2) receptor antagonists
  2. sucralfate
  3. proton pump inhibitors (omeprazole)
  4. antacids
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33
Q

What are the 8 clinical uses of drugs that treat GI ulcers?

A
  1. gastritis
  2. gastric ulcers
  3. duodenal ulcers
  4. GI ulcer prevention
  5. esophagitis
  6. mast cell tumors
  7. hypergastrinemic syndromes
  8. prevention and treatment of NSAID-induced ulcers
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34
Q

How does HCl secretion in carnivores compare to humans?

A

carnivores = intermittent
humans = continuous

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35
Q

In which animals is GI ulceration most prevalent? What are 7 contributing factors?

A

horses
1. stall confinement
2. intense exercise
3. diet (high energy concentrated)
4. racing stress
5. intermittent feeding schedule
6. increased stomach acidity
7. use of NSAIDs

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36
Q

How do antacids work to treat GI ulcers? What are 4 examples?

A

neutralize stomach acid through a simple reaction to form water and neutral salt

  1. magnesium hydroxide
  2. aluminum hydroxide
  3. calcium carbonate
  4. sodium bicarbonate
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37
Q

Antacids have no systemic effects. What 3 local effects do they have?

A
  1. decrease pepsin activity
  2. bind bile acids in stomach
  3. stimulates local prostaglandin synthesis
38
Q

Why are adverse effects rare when using antacids? What are 2 possible adverse effects?

A

seldom administered long-term and are not absorbed

  1. magnesium accumulation can be dangerous in patients with kidney disease
  2. interfere with the oral absorption of other drugs —> chelates with fluoroquinolones or tetracyclines (AB must be administered 2 hr before)
39
Q

What 4 histamine (H2) receptors antagonists are used to treat GI ulcers? How do they work?

A
  1. Cimetidine
  2. Ranitidine
  3. Famotidine
  4. Nizatidine

reversible, competitive inhibitors that reduce the amount of hydrogen ion content in the gastric acid secretions (lowers acidity) and the amount of pepsine

40
Q

Activation of what 3 receptors stimulate acid secretion?

A
  1. gastrin receptors: endocrine CCK
  2. H2: paracrine
  3. M3: neuronal ACh
41
Q

Which 2 of the histamine (H2) receptor antagonists have prokinetic effects? Why?

A
  1. Ranitidine
  2. Nizatidine

inhibit anticholinesterase (AChE) activity = prokinetic at antisecretory doses

42
Q

How long does it take for histamine (H2) receptor antagonists to work?

A
  • clinical signs of ulceration resolve within a few days
  • complete healing takes 10-14 days
43
Q

How does absorption of histamine (H2) receptor antagonists compare in horses and dogs? Which one is most commonly used in horses?

A

not absorbed as well in horses as well in dogs

Ranitidine

44
Q

What 2 histamine (H2) receptor antagonists are used in calves? What are they used for?

A

Cimetidine and Ranitidine

maintain pH of the abomasum > 3.5

45
Q

What are the main 2 adverse effects of histamine (H2) receptor antagonists?

A
  1. Cimetidine can inhibit the clearance of other drugs
  2. impairs the oral absorption of drugs that require acidity
46
Q

How does sucralfate work to treat GI ulcers?

A
  • dissociates in the acid milieu of the stomach into sucrose octasulfate and aluminum hydroxide
  • sucrose octasulfate polimerizes into a viscous, sticky substance that binds to ulcerated mucosa
  • also increases mucosal synthesis of prostaglandins for protection, inactivates pepsin, and absorbs bile acid
47
Q

What drug interaction does sucralfate have?

A

resulting dissociation producing aluminum hydroxide can chelate with fluoroquinolone and tetracycline (administer AB first, 30 mins to 2 hrs before)

48
Q

What are the most potent antisecretory drugs used for treating GI ulcers? How do they work?

A

proton pump inhibitors (PPIs) - Omeprazole

  • weak bases that act as prodrugs in the physiological pH of the blood
  • after systemic absorption, they become trapped in the acidic parietal cells in the stomach
  • irreversible antagonists of the H+/K+ ATPase pump
49
Q

Why is the effect of protein pump inhibitors prolonged?

A

acid secretion only resumes after new proton pumps are synthesized in the parietal cells, which usually takes 24-48 hrs

50
Q

What are 3 indications for proton pump inhibitors? When are they given to ensure maximal absorption?

A
  1. support gastroduodenal healing
  2. prevention/treatment of gastroesophageal reflux
  3. treatment of hypersecretory conditions

acid secretion is activated by ingestion of a meal —> give 30 mins to an hr prior

51
Q

What secondary effect do proton pump inhibitors have?

A

inhibits a variety of CYP —> caution with combining other drugs metabolized by the liver

52
Q

What are 4 possible adverse effects of chronic administration of proton pump inhibitors?

A
  1. loss of negative feedback mechanisms results in elevated gastrin levels, which exerts a hypertrophic effect on the gastric mucosa
  2. small intestinal bacterial overgrowth (SIBO) due to an increase in stomach pH, which can result in malabsorption syndromes and impaired vitamin B12 absorption (increased Lactobacillus, decreased Helicobacter)
  3. diarrhea most common in dogs
  4. transient fluctuations in liver enzymes
53
Q

How do synthetic prostaglandins work to treat gastric ulcers? How are they used in dogs?

A

(Misoprostol)
E prostaglandins inhibit gastric acid secretion by blocking cAMP production through EP3 receptors on parietal cells

prevents duodenal hemorrhage and ulceration associated with aspirin therapy

54
Q

When does Misoprostol work best for GI ulcers? What does it inhibit? When is use contraindicated?

A

prevention of GI ulcers, less beneficial for treating ulcers once they occur

basal, nocturnal, and food-induced gastric acid secretion

pregnant patients - can induce uterine contractions

55
Q

What bacteria most commonly causes gastritis and ulcers in animals? What is the best way to treat?

A

Helicobacter pylori and Helicobacter-like organisms

combination of metronidazole and/or clarothromycin plus amoxicillin, and PPI or H2-receptor antagonist

56
Q

Drugs for treatment of GI ulcers:

A
57
Q

What is diarrhea? What is the difference between acute and chronic?

A

increase in fecal water content resulting in increased frequency, volume, or fluidity of feces

  • ACUTE: sudden onset in a previously healthy animal, 3 days - 2 weeks, self-limiting, resolves without consequence
  • CHRONIC: 3-4 weeks, recurring passage of diarrheal stool, fever, loss of appetite, nausea, vomiting, weight loss, chronic weakness
58
Q

What are the 4 most important treatments for diarrhea? Why do many causes of diarrhea not require drug therapy?

A
  1. fluid therapy
  2. electrolyte replenishment
  3. maintaining acid/base balance
  4. discomfort control

most causes are self-limiting

59
Q

How do mucosal protectants and adsorbents work to treat diarrhea?

A

PROTECTANTS produce a coating of the GI epithelium that prevents irritation or erosion by potentially harmful substances

ADSORBENTS bind chemical compounds to prevent their absorption and cause their elimination in the feces

(kaolin-pectin, bismuth subsalicylate)

60
Q

How does kaolin-pectin work? How can it affect stool? What formulation is most common?

A

binds bacterial toxins in the GI tract (adsorbent)

may change consistency - no decrease in fluid or electrolyte loss or illness duration

Kao-Pectate, containing salicylate
- pectin may bind other drugs given orally

61
Q

What is the most useful symptomatic treatment of acute diarrhea? How does it work?

A

bismuth subsalicylate - PeptoBismol

adsorbs bacterial enterotoxins and produces some gastric intestinal protection

62
Q

What do the active ingredients in PeptoBismol do? How can it affect stool?

A
  • salicylate is absorbed systemically in dogs and cats (unlikely to cause toxicity)
  • bismuth can an anti-Helicobacter effect in the stomach

may turn it black

63
Q

What motility modifiers are used to treat diarrhea? What 3 effects do they have?

A

anticholinergic (antimuscarinic) drugs —> M1 and M3 antagonists

  1. decrease intestinal motility and secretions
  2. decrease fluid secreted into the bowel
  3. decrease abdominal discomfort
64
Q

What is the stovepipe effect?

A

with some forms of diarrhea, the usage of anticholinergic drugs to modify motility of the GI tract can worsen conditions, especially in infectious diarrhea (Salmonella)

65
Q

What are 5 possible adverse effects of anticholinergic motility modifiers used to treat diarrhea? When is usage contraindicated?

A

SYSTEMIC
1. ileus
2. xerostomia
3. urine retention
4. cycloplegia
5. tachycardia

chronic administration can lead to stomach distension and discomfort —> don’t use in patients with gastritis and vomiting

66
Q

How can CNS excitement be avoided when using anticholinergic motility modifiers to treat diarrhea?

A

administer quarternary amines that have lower lipophilicity compared to tertiary amines (atropine, scopolamine), so they cannot cross the BBB

67
Q

What is N-butylscopolammonium bromide (Buscopan)? What is the most common adverse effect? When is usage contraindicated?

A

antispasmodic (anticholinergic) drug used to treat colic in horses and relax the large bowel for rectal examination and colonoscopy

increased heart rate lasting 30 mins

horses with impaction or ileus

68
Q

What endogenous opioids are present in the intestinal walls? How does location compare in dogs and cats?

A

enkephalins, β-endorphin, dynorphin

DOGS: enkephalin neurons are in the submucosal plexus
CATS: enkephalin detected in both myenteric and submucosal plexuses

69
Q

Where do opioids act in the GI tract? What are the 4 main effects?

A

µ (OP3) and ð (OP1) opiate receptors

  1. decrease propulsive intestinal contractions
  2. increase tone of GI sphincters
  3. antisecretory
  4. stimulate absorption of fluid, electrolytes, and glucose
70
Q

How do opioids help treat secretory diarrhea?

A

inhibit calcium influx and decreases calmodulin activity

71
Q

What are the 2 most common opioids used to treat diarrhea?

A
  1. diphenoxylate hydrochloride - meperidine derivative that dries salivary secretions (discourage human abuse) and is able to cross the BBB (systemic effects
  2. loperamide hydrochloride - butyramide derivative most commonly used (OTC), without systemic effects (P-gp keeps from crossing BBB), increases intestinal transit time and luminal capacity
72
Q

Why are opioids contraindicated in infectious diarrhea?

A

opiates may significantly slow the GI tract and increase the absorption of bacterial toxins

73
Q

What most commonly causes bacterial diarrhea in large animals? Why is antimicrobial usage questioned?

A

E. coli (not a common problem in small animals)

  • may worsen diarrhea by suppressing normal microflora
  • AMR: base antibiotic choice on IBI, fecal gram staining
74
Q

How do enterotoxins affect the intestine? What are the 3 major signs of mucosal damage?

A

stimulate intestinal secretions by producing cAMP

  1. hemorrhagic diarrhea
  2. fever
  3. abdominal white blood cells count
    - THIS is when systemic AB therapy is indicated
75
Q

What antimicrobials are recommended for Salmonella, Campylobacter jejuni, E. coli, and Clostridium perfringens infections?

A

SALMONELLA: enrofloxacin, trimethoprim-sulfonamide

C. JEJUNI: erythromycin, furazolidone, doxycycline

E. COLI: enrofloxacin

C. PERFINGENS: tylosin***, amoxicillin, ampicillin, metronidazole, clindamycin

76
Q

In what 4 conditions is it common to use Tylosin to treat diarrhea?

A
  1. chronic diarrhea in dogs
  2. affects both large and small bowels
  3. specific etiology is not identified
  4. Campylobacter jejuni and Clostridium perfringens have been isolated
77
Q

What are the 4 most common causes of inflammatory intestinal disease? What is IBD characterized by?

A
  1. parasites
  2. bacteria
  3. food hypersensitivity
  4. immune-mediated diseases

infiltraction of inflammatory cells in the gastric or intestinal mucosa
- lymphocytic, plasmacytic, eosinophilic, neutrophilic

78
Q

What are the general steps for medical management of inflammatory intestinal disease?

A
  • antiparasitic therapy
  • dietary therapy (elimination diet)
  • probiotics
  • ALL ELSE FAILS: anti-inflammatory drugs
79
Q

What is Sulfasalazine? How does it work? How does it affect the intestine?

A

combinaion of sulfapyridine and 5-aminosalicylic acid (mesalamine) used to treat colitis (not as effective in small intestine)

sulfonamide is absorbed into circulation and salicyclic acid remains active to inhibit prostaglandin (antilipooxyhenase) and decrease intestinal oxygen free radicals

80
Q

When is the usage of Sulfasalazine contraindicated?

A

(antiinflammatory)
- patients with allergic reactions to sulfonamides
- can cause keratoconjunctivitis sicca

81
Q

How are inflammatory intestinal diseases diagnosed?

A

biopsy —> identified predominant inflammatory cells

82
Q

What glucocorticoid is commonly used to treat inflammatory intestinal disease? How does it work?

A

Prednisolone

suppress cytokine synthesis, leukocyte migration, and lymphocyte activation
- Budesonide in humans (maybe animals?)

83
Q

What immunosuppressive can be used to treat inflammatory intestinal disease? How does it work?

A

Azathioprine

metabolized into active metabolites that inhibit activated lymphocytes
- dogs with severe inflammatory bowel disease

84
Q

What N-3 fatty acid is used to treat colitis?

A

eicosapentaenoic acid
- people
- supplementation for 4 months reduces leukotriene levels in the colon

85
Q

What do laxatives and cathartics? What are 5 common types?

A

drugs that increase motility of bowel and change the character of the stool

  1. bulk-forming laxatives
  2. stool softener
  3. lubricants
  4. saline hyperosmotic agents
  5. stimulants
    (soften stool, increase fluid content of stool)
86
Q

How do stimulant (irritant) laxatives work? What is a common adverse effect?

A

Anthraquinone - causes electrolyte loss by inhibiting Na+/K+ ATPase in the intestine

chronic use = enterocyte damage

87
Q

How do hyperosmotic cathartics work? What are they most commonly used for?

A

saline - nonabsorbed electrolytes draw fluid into the bowel via osmosis, causing the intestine to dilate and increase normal peristalsis

  • prepare animals for endoscopic procedures
  • poisoning treatment
88
Q

How do bulk-forming laxatives work?

A

dietary plant fibers —> carboxymethylcellulose

nonabsorbed synthetic or natural polysaccharide and cellulose derivatives that are resistant to digestion and attract water into the intestine (slow acting)

89
Q

How do lubricants work as laxatives? What are they specifically used for in horses/cattle and cats?

A

mineral oil, liquid petrolatum (vaseline)

coat the surface of the stool with a water-immiscible film to increase the water content of the stool

HORSES/CATTLE = mineral oils help with nonspecific GI problems
CATS = increase the passage of trickobezoars (hair balls)

90
Q

How do stool softeners (surfactants) work? What are 4 examples?

A

decrease surface tension and allow more water to accumulate in the stool

  1. Docusate sodium/calcium
  2. bile acids (dehydrocholic/ursodeoxycholic acid) - increases bile flow, laxative, improves liver disease (UDCA)
  3. castor oil - hydrolyzed in bowel and releases ricinoleic acid causing increased secretion of water
91
Q

True or false: Regarding PPIs, the binding to the carrier is irreversible and restoration of acid secretion requires de novo synthesis of ATPase by the parietal cell.

A

TRUE

Introduction to Pharmacology (39 decks)

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