GI Meds Flashcards

(48 cards)

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
Antacid types
- Al (aluminum related compounds) - Mg (milk of magnesia) - CaCO3 (Tums) - NaHCO3 (Baking soda, alka seltzer)
26
Antacid combo examples
- Maalox --> Al3+ & Mg2+ - Mylanta --> CaCO3 & Mg(OH)2
27
Anticholinergics for ulcer disease effects AEs
- Pirenzepine - produces selective blockage of M receptors that regulate gastric secretion - AEs: dry mouth, constipation, N/V/D
28
Laxative types (6)
- Bulk - Surfactant - Lubricant - Osmotic - Stimulant - Serotonin Receptor agonist
29
Bulk laxatives effects/AEs
ex. Metamucil - increases volume/stretches intestinal wall stimulating peristalsis - used in IBS, diverticulosis, diarrhea - **AEs: esophageal obstruction if not taken with water
30
Surfactant laxative effect
ex. Docusate/Colace - lowers surface tension of stool, facilitates water penetration; inhibits fluid absorption & stimulates secretion of water/electrolytes into intestine
31
Lubricant laxative ex.s
- glycerin suppository & mineral oil
32
Osmotic laxative effect
ex. Milk of magnesia, Sorbitol, Lactulose - increases liquidity of stool due to increase stool fluid
33
stimulant laxatives effects
ex. Bisacodyl/Dulcolax, Senna, Castor oil - acts on small intestine/colon to produce soft/semi fluid stool
34
Serotonin receptor agonist laxatives effects and AEs
ex. Tegaserod - 5HT4 partial agonist --> stimulates peristalsis, increases stool liquidity - AEs: diarrhea, resolves alone - restricted use for IBS
35
Anti-diarrheal agents (3)
- opioids - loperamide - Diphenoxylate
36
tri-cyclic anti-depressants in IBS moa
- alter central processing of visceral afferent info - anticholinergic effects leads to motility and secretion - decreases nociception
37
Serotonin 5HT3 receptor agonist in IBS moa/AEs
- 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
antispasmodics (anticholinergics) in IBS moa
- 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
Probiotics
- 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
Probiotics AEs
- gas, bloating, diarrhea, eructations - usually mild/transient - infectious complications have occurred in highly immunosuppressed/critically ill pts
41
sulfasalazine use/Aes
- 5-aminosalicylate used for Crohns/UC - suppresses prostaglandin synthesis and migration of inflammatory cells into area - AEs: N, fever, rash, arthralgia, hematologic disorders
42
Anti-Emetics: 5HT3 receptor blocker
ex. Ondansetron SE: HA, diarrhea, dizziness - useful for chemo tx induced and post op N/V
43
Anti-Emetics: Substance P/Neurokinin antagonist
ex. Aprepitant - prevents acute & delayed N/V - inhibitor and inducer of CYP3A4
44
Anti-Emetics: Prokinetic agents
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
Anti-Emetics: muscarinic antagonist
*most useful for motion sickness - block M and H1 - SE: sedation, dry mouth, blurred vision
46
Anti-Emetics: benzodiazepines
- suppresses anticipatory vomiting in chemo
47
Anti-Emetics: glucocorticoids
- moa unknown
48
Anti-Emetics: phenothiazines
- D2 blocker SE: EPS, anticholinergic effects, hypotension, sedation