GI Meds Flashcards

1
Q

Antibiotic choices to treat H. Pylori

A
  • Amoxicillin
  • Clarithromycin
  • Metronidazole
  • Tetracycline

**must be used in some form of combo

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2
Q

Bismuth for treatment of H. Pylori MoA

A
  • disrupts cell wall
  • inhibits urease activity
  • likely creates protective later in stomach, bicarb/mucus secretion
  • decreases stool liquidity
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3
Q

1st choice drug class to treat ulcers

A

Histamine2 receptor antagonists –> suppress secretion of gastric acid

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4
Q

Histamine 2 receptor antagonist drugs (H2RAs)

A
  • Cimetidine
  • Famotidine
  • Nizatidine
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5
Q

Cimetidine MoA

A
  • blocks H2 receptors, decreasing volume of gastric juice and [H+ ion]; reversible process
  • effective specifically against nocturnal acid secretion; suppresses basal acid secretion
  • cross BBB –> CNS effects
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6
Q

Cimetidine uses

A
  • GERD
  • gastric/duodenal ulcers
  • Zollinger-Ellison syndrome
  • aspiration pneumonitis
  • heartburn
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7
Q

Cimetidine AEs

A

Binds to androgen receptors producing blockade
- gynecomastia, reduced libido, impotence
- CNS: confusion, hallucinations, depression, or excitation
- IV hypotension and dysrhythmias
*CYP inhibitor

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8
Q

opioids and antacids

A
  • inhibitory property of antacids leads to better high in opiate use
  • increasing stomach pH allows for better opiate absorption/longer high
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9
Q

Famotidine & Nizatidine differences from Cimetidine

A
  • more potent and fewer drug interactions than Cimetidine
  • no effect on H1 receptors; absorbed w/ or w/o food
  • less CNS effects, no androgen binding
  • weak CYP inhibition
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10
Q

Famotidine & COVID 19

A
  • in adults with mild-mod covid-19, tx with high dose famotidine led to early resolution of symptoms and inflammation
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11
Q

long term H2RA safety issues

A
  • cognitive impairment –> linked to dementia
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12
Q

Most effective class of drugs to suppress gastric acid secretion

A
  • PPIs/proton pump inhibitors
    *End in -prazole
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13
Q

Proton pump inhibitor (PPIs) drugs

A
  • Omeprazole
  • Esomeprazole
  • Lansoprazole
  • Rabeprazole
  • Pantoprazole
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14
Q

Omeprazole moa

A
  • prodrug converted to active form inside parietal cell
  • causes irreversible inhibition of H+, K+, ATPase and lasts until new one is synthesized
  • inhibits basal and stimulated acid release
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15
Q

omeprazole uses

A
  • ulcers
  • GERD
  • hypersecretory conditions
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16
Q

omeprazole AEs

A

HA, diarrhea, N/V, long term risk of CA

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17
Q

omeprazole d-d interactions

A
  • affects absorption of atazanacir, ketoconazole, itraconazole due to increased gastric pH
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18
Q

Long term PPI safety (endocrine/nutritional/Hip fx)

A
  • Endo: elevated serum gastric levels
  • Nutrition: can lower B12 absorption
  • Hip Fx: higher dose = higher risk; presumed that cid inhibition interferes with Ca2+ absorption in small intestine
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19
Q

Long term PPI safety (C. Diff, Plavix, CKD)

A
  • CA-C. diff: theorized that decrease in gastric acidity may be “permissive” to enteric infection
  • Plavix: omeprazole reduces efficacy; pantoprazole less likely to do so
  • CKD: significantly higher incidence of CKD in PPI users
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20
Q

Long term PPI safety (Cognition & pediatric use)

A
  • Cognition: long term use linked to dementia
  • Peds: use of lansoprazole in poorly controlled asthma showed no improvement; increased respiratory symptoms and community acquired pneumonia
21
Q

H. Pylori newest tx regimen (2)

A
  • Quadruple therapy (PBMT)
    –> PPI, Bismuth, Metronidazole & Tetracycline
    OR
  • Concomitant therapy (PAMC)
    —> PPI, Amoxicillin, Metronidazole, Clarithromycin
22
Q

Sucralfate use

A
  • mucosal protective agent
  • other ulcer tx drug
  • binds to actual ulcer, MoA unknown
23
Q

Misoprostol moa/use/AEs

A
  • prostaglandin analog
  • other ulcer tx drug
  • moa: inhibits acid and protects mucosal lining; short half life, freq. dosing needed
  • use: NSAID induced ulcers
  • AE: stimulates uterine contractions, abd pain, diarrhea (often using in L&D!)
24
Q

Antacids effects

A
  • neutralize stomach acid; different capacities depending on the compound
  • enhances mucosal protection by stimulating PG production, used for ulcers
  • symptomatic relief, doesnt accelerate healing
25
Q

Antacid types

A
  • Al (aluminum related compounds)
  • Mg (milk of magnesia)
  • CaCO3 (Tums)
  • NaHCO3 (Baking soda, alka seltzer)
26
Q

Antacid combo examples

A
  • Maalox –> Al3+ & Mg2+
  • Mylanta –> CaCO3 & Mg(OH)2
27
Q

Anticholinergics for ulcer disease effects AEs

A
  • Pirenzepine
  • produces selective blockage of M receptors that regulate gastric secretion
  • AEs: dry mouth, constipation, N/V/D
28
Q

Laxative types (6)

A
  • Bulk
  • Surfactant
  • Lubricant
  • Osmotic
  • Stimulant
  • Serotonin Receptor agonist
29
Q

Bulk laxatives effects/AEs

A

ex. Metamucil
- increases volume/stretches intestinal wall stimulating peristalsis
- used in IBS, diverticulosis, diarrhea
- **AEs: esophageal obstruction if not taken with water

30
Q

Surfactant laxative effect

A

ex. Docusate/Colace
- lowers surface tension of stool, facilitates water penetration; inhibits fluid absorption & stimulates secretion of water/electrolytes into intestine

31
Q

Lubricant laxative ex.s

A
  • glycerin suppository & mineral oil
32
Q

Osmotic laxative effect

A

ex. Milk of magnesia, Sorbitol, Lactulose
- increases liquidity of stool due to increase stool fluid

33
Q

stimulant laxatives effects

A

ex. Bisacodyl/Dulcolax, Senna, Castor oil
- acts on small intestine/colon to produce soft/semi fluid stool

34
Q

Serotonin receptor agonist laxatives effects and AEs

A

ex. Tegaserod
- 5HT4 partial agonist –> stimulates peristalsis, increases stool liquidity
- AEs: diarrhea, resolves alone
- restricted use for IBS

35
Q

Anti-diarrheal agents (3)

A
  • opioids
  • loperamide
  • Diphenoxylate
36
Q

tri-cyclic anti-depressants in IBS moa

A
  • alter central processing of visceral afferent info
  • anticholinergic effects leads to motility and secretion
  • decreases nociception
37
Q

Serotonin 5HT3 receptor agonist in IBS moa/AEs

A
  • drug: Alosteron
  • blocks receptors in gut on way to spinal cord inhibiting sensation of N, pain and bloating-slowsclonic transit
  • AEs: constipation requiring hospitalizations, ischemic colitis
38
Q

antispasmodics (anticholinergics) in IBS moa

A
  • Dicyclomine, Hyoscyamine
  • inhibits muscarinic cholinergic receptors in the enteric plexus/on smooth muscle
  • low doses, minimal ANS effects; high doses = dry mouth, visual disturbances, urinary retention
39
Q

Probiotics

A
  • dietary supplements thought to inhibit bacterial toxins, lower pH, and inhibit growth of pathogenic bacteria; physically/chemically prevent adhesion and colonization of pathogenic bact.
40
Q

Probiotics AEs

A
  • gas, bloating, diarrhea, eructations
  • usually mild/transient
  • infectious complications have occurred in highly immunosuppressed/critically ill pts
41
Q

sulfasalazine use/Aes

A
  • 5-aminosalicylate used for Crohns/UC
  • suppresses prostaglandin synthesis and migration of inflammatory cells into area
  • AEs: N, fever, rash, arthralgia, hematologic disorders
42
Q

Anti-Emetics: 5HT3 receptor blocker

A

ex. Ondansetron
SE: HA, diarrhea, dizziness
- useful for chemo tx induced and post op N/V

43
Q

Anti-Emetics: Substance P/Neurokinin antagonist

A

ex. Aprepitant
- prevents acute & delayed N/V
- inhibitor and inducer of CYP3A4

44
Q

Anti-Emetics: Prokinetic agents

A

ex. Metoclopramide
- suppresses emesis by blocking 5HT & DA; increases upper GI motility by enhancing actions of ACh
- uses: GERD, DM gastroparesis, N/V r/t chemo or post-op
- SEs: EPS, BBW–> tardive dyskinesia, sedation

45
Q

Anti-Emetics: muscarinic antagonist

A

*most useful for motion sickness
- block M and H1
- SE: sedation, dry mouth, blurred vision

46
Q

Anti-Emetics: benzodiazepines

A
  • suppresses anticipatory vomiting in chemo
47
Q

Anti-Emetics: glucocorticoids

A
  • moa unknown
48
Q

Anti-Emetics: phenothiazines

A
  • D2 blocker
    SE: EPS, anticholinergic effects, hypotension, sedation