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Pharmacology > GI Drugs > Flashcards

GI Drugs Flashcards

1
Q

what do acid peptic diseases compose of

A

peptic ulcer (duodenal and gastric), gastroesophageal reflux, zollinger ellison syndrome (ZES)

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2
Q

pathologies that causes peptic ulcers

A
  • gastric acid
  • decreased mucosal resistance to acid
  • H pylori infection
  • NSAIDs
  • concurrent use of warfarin and corticosteroids
  • stress esp if older than 65
  • lifestyle
  • gastrinoma - gastrin secreting tumor
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3
Q

what do peptic disease do to the surface of GI tract

A

erodes and ulcerates the mucosal lining

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4
Q

therapeutic choices for peptic ulcer diseases and their functions

A

A HAM

  • Antacids: neutralizes acid
  • H2 antagonist and Proton Pump Inhibitor - reduces gastric acid secretion
  • Antimicrobial treatments - eradicate H pylori infection
  • Mucosal protective agents - augment mucosal surface defense
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5
Q

mechanism of gastric antacids

A

they are weak bases that react with gastric HCl to form water and salt –> increase in pH –> quick relief of symptoms

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6
Q

name the antacids

A

CAM

Calcium Carbonate
Aluminum Hydroxide
Magnesium Hydroxide

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7
Q

adverse effects of each antacids

A
  • Calcium Carbonate –> Hypercalcemia which leads to nephrolithiasis and constipation –> fecal compaction
  • Aluminum Hydroxide –> form aluMINIMUM chloride that is insoluble –> MINIMUM amount of feces –> constipation and Hypophosphatemia
  • Magnesium Hydroxide –> for Mg salt which is poorly absorbed and causes diarrhea (Mg – Must go to the bathroom)
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8
Q

clinical correlates of antacids and drug absorption

A
  • increases oral absorption of weak bases (quinidine)
  • decreases oral absorption of weak acids (warfarin)
  • decreases oral absorption of Ca, Mg, and Al molecules –> chelate tetracycline
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9
Q

what are some factors that enhance gastric acid secretion and via what mechanism

A

Histamine, Acetylcholine, and Gastrin via H+/K+ ATPase pump

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10
Q

what are the H2 receptor blockers

A

FRaNC

Famotidine
Ranitidine
Nizatidine
Cimetidine

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11
Q

how effective are H2 receptor blockers/mechanism

A

they are effective at decreasing gastric acid secretion but have no effect on gastric emptying time

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12
Q

of all the H2 receptor blockers, which ones are longer acting/more potent

A

all but cimetidine

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13
Q

clinical uses of H2 receptor blockers

A
  • promote healing of duodenal and gastric ulcers
  • relieve gastro esophageal reflux
  • given preoperatively to prevent aspiration pneumonia
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14
Q

adverse effects of H2 blockers excluding cimetidine

A

nausea, headache, dizziness

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15
Q

adverse of H2 blocker cimetidine

A
  • inhibitor of CYP450 enzymes
  • antiandrogenic effects - gynecomastia, elevated prolactin levels, decreased libido
  • confusion in older people
  • decrease renal excretion of creatinine
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16
Q

since Cimetidine is a CYP450 inhibitor, what drugs does it affect

A
  • warfarin
  • procainamide
  • phenytoin
  • benzos
  • theophylline
  • imipramine
  • quinidine
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17
Q

what are the proton pump inhibitors

A

PROLE PRAZOLES

  • Pantoprazole
  • Rabeprazole
  • Omeprazole
  • Lansoprazole
  • Esomeprazole
18
Q

mechanism of proton pump inhibitors

A

in parietal cells, they are converted to their active form –> reacts with cysteine on H+/K+ ATPase –> form stable covalent bond –> irreversible inactivation of enyzme

19
Q

clinical uses of proton pump inhibitors

A
  • GERD, duodenal and gastric ulcers, multiple endocrine neoplasia 1 (MEN-1), Zollinger Ellison
  • together with antibiotics help with H pylori infection
  • NSAIDs induced ulcers: not only inhibit proton release but also they support platelet aggregation and maintain clot integrity (hemorrhagic ulcers usage)
20
Q

adverse effects of proton pump inhibitors

A
  • omeprazole inhibits metabolism of warfarin, clopidogrel, phenytoin, diazepam, cyclosporine
  • decrease bioavailability of vit B12
  • acid needed for absorption of digoxin and ketocanozole so decreased absorption of them
  • long term use of omeprazole –> gastric carcinoid tumor
21
Q

how do you diagnose H pylori infection

A
  • endoscopic biopsy of ulcer margin
  • serology test
  • urea breath test
22
Q

first line antimicrobials for H pylori eradication

A 
CAMT
Clarithromycin
Amoxicillin
Metronidazole
Tetracycline
23
Q

what are the mucosal protective agents

A

Mucosal MoBS

Misoprostol
Bismuth Subsalicylate
Sucralfate

24
Q

mechanism of sucralfate

A
  • binds to necrotic tissue and acts as a barrier to acid

- stimulates prostacyclin synthesis

25
Q

when is sucralfate ineffective and why

A

with use of H2 receptor blocker or PPIs or antacids because it needs an acidic environment (low pH) to be activated

26
Q

mechanism of bismuth subsalicylate

A

binds to ulcers and forms a coating and protects it from acid and pepsin

27
Q

extra effects of bismuth subsalicylate

A

has some antimicrobial effects against H. pylori

28
Q

mechanism of misoprostol

A

prostaglandin analogue (eicosanoid) that decreases acid secretion, stimulates mucin and bicarb secretion

29
Q

clinical use of misoprostol

A

prevention of gastric ulcers induced by NSAIDS

30
Q

adverse effects of misoprostol

A

DAE

  • diarrhea
  • abortion
  • exacerbates IBD
31
Q

cause of gastroesophageal reflux

A

abnormal relaxation of lower esophageal sphincter which allows acids from stomach to get to the esophagus

32
Q

risk factors for gastroesophageal reflux

A

obesity, drugs, zollinger ellison, increased BMI

33
Q

treatment of gastroesophageal reflux

A
  • nonpharmacological: lose weight, don’t drink acid rich drinks before bed, sleep with head elevated, small meals, stop smoking and drinking
  • antacids: neutralize acid
  • PPIs and H2 blockers
34
Q

what are the prokinetic drugs

A
  • Cholinomimetics: neostigmine, bethanechol
  • 5-HT agonists: metoclopramide, cisapride
  • Macrolides: erythromycin
35
Q

importance of prokinetic drugs

A

relieve GI symptoms of abdominal discomfort, bloating, heart burn, nausea, vomiting etc

36
Q

mechanism of pro kinetic activity of metoclopramide

A

muscarinic activity via 5-HT4 receptor agonist activity

37
Q

clinical use of metoclopramide

A
  • diabetic, post op gastroparesis, and relief of symptoms of GERD
  • nausea and vomiting for those on chemo
38
Q

adverse effects of metoclopramide

A

anti dopaminergic

  • sedation
  • diarrhea
  • Parkinsonian effects
39
Q

mechanism of cisapride and use

A

5-HT4 agonist that stimulates ACh –> treatment of gastroparesis, GERD, constipation

40
Q

adverse effect of cisapride

A

cardiac effects - arrhythmias

Pharmacology (79 decks)

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