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Pharm > Upper GIT Drugs > Flashcards

Upper GIT Drugs Flashcards

1
Q

Acid Peptic Disorders

Corroding vs Protective factors

A
  • Corroding
    • Gastric acid
    • Pepsin
    • Bile
    • Helicobacter Pylori
  • Protective
    • Secretion of mucus and bicarbonate
    • Blood flow
    • Mucosal cellular regeneration
    • Prostaglandins
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2
Q

GERD becomes pathological when there is … (2)

A

Macroscopic damage to the esophagus.

AND/OR

Symptoms which reduce quality of life

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3
Q

List the symptoms of GERD

A
  • Heartburn
  • Regurgitation
  • Water brash
  • Dysphagia
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4
Q

list the complications of GERD

A
  • Barret’s esophagus
  • Esophageal carcinoma
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5
Q

Peptic Ulcer Disease (PUD) is ____ erosions d/t corroding factors overwhelming protective factors

A

Peptic Ulcer Disease (PUD) is mucosal erosions d/t corroding factors overwhelming protective factors

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6
Q

Gastric ulcers from NSAID use and epigastric pain is _____ by eating

whereas

Duodenal ulcers from H. pylori infection, epigastric pain ____ by eating

A

Gastric ulcers from NSAID use and epigastric pain is worsened by eating

whereas

Duodenal ulcers from H. pylori infection, epigastric pain relieved by eating

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7
Q

Describe the complications of peptic ulcer disease

A
  • Can be life-threatening
  • upper G.I. bleeding
  • gastric/duodenal perforation
  • gastric outlet obstruction
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8
Q

Regulation of gastic acid secretion has ____ overlapping mechanisms: (list the 3)

A

Regulation of gastic acid secretion has redundant overlapping mechanisms: Endocrine, Paracrine, Neural

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9
Q

Describe the image

A

Two major physiological states of gastric acid production: Basal & Meal stimulated

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10
Q

Antacids are weak ____ obtained without prescription

A

Antacids are weak bases obtained without prescription

Antacid + HCl → salt + H2O

Therapeutic neutralization of low gastric pH protects esophageal mucosa from reflux corrosion

Time of onset: 5 minutes
Duration of action: 30 mins – 1 hour

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11
Q

Antacids can affect absorption, bioavailability, or urinary excretion of other drugs by ____ gastric and urinary pH or by _____ gastric emptying.

All can cause ____.

A

Antacids can affect absorption, bioavailability, or urinary excretion of other drugs by increasing gastric and urinary pH or by delaying gastric emptying.

All can cause hypokalemia.

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12
Q

(Antacids)

Aluminum Hydroxide causes ____

Magnesium Hydroxide causes ____

therefore, combined to produce _____

A

(Antacids)

Aluminum Hydroxide causes constipation
“Aluminimum amount of feces”

Magnesium Hydroxide causes osmotic diarrhea
“Must _g_o 2 the washroom (Mg2+)”

Al and Mg combined to produce no change in bowel movements

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13
Q

Calcium Carbonate is an ____, CO2 causes _____, can lead to metabolic _____, aka ____ syndrome.

A

Calcium Carbonate is an antacid, CO2 causes belching, can lead to metabolic alkalosis, aka milk alkali syndrome.

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14
Q

describe antacid drug interactions

A
  • Binding/ chelation of many drugs
  • Increased gastric pH alters dissolution of weakly charged drugs
  • Decreased absorption of co-administered
    • tetracyclines
    • fluoroquinolones
    • itraconazole
    • iron
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15
Q

H2 receptor antagonists suppress _____ and reduce signal transduction for ____ and ____-induced gastric acid production.

A

H2 receptor antagonists suppress histamine-induced gastric acid secretion, and reduce signal transduction for ACh and Gastrin-induced gastric acid production.

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16
Q

H2 receptor antagonists are highly selective _____ inhibitors at the ____ cell H2 Gs protein coupled receptor

Time of onset: 2.5 hours
Duration of action: 4- 10 hours
_____ develops in 2- 6 weeks

A

H2 receptor antagonists are highly selective competitive inhibitors at the parietal cell H2 Gs protein coupled receptor

Time of onset: 2.5 hours
Duration of action: 4- 10 hours
Tachyphylaxis develops in 2- 6 weeks

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17
Q

list the H2 Receptor Antagonists

A
  • Cimetidine – prototype with many adverse effects
  • Ranitidine, Famotidine, Nizatidine – 2nd generation with no anti-androgenic or CNS adverse effects
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18
Q

describe the effect of H2RAs on Gastric Acid Secretion

A
  • H2RAs strongly suppress basal gastric acid secretion
  • Modest effect on meal stimulated secretion
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19
Q

list the H2 receptor antagonist indications

A
  • GERD
  • PUD
  • Nonulcer dyspepsia
  • Prophylaxis against stress-related gastritis
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20
Q

what is the only H2 receptor antagonist with adverse effects

A

CIMETIDINE

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21
Q

AEs of Cimitidine

A
  • acts as nonsteroidal anti-androgen and prolactin stimulant → gynecomastia, galactorrhea, and male impotence
  • Crosses BBB → confusion, dizziness and headaches
  • Increases gastric pH → B12 deficiency and myelosuppression (long term use)
  • Potent CYP450 inhibitor increasing serum [] of:
    • Warfarin, Diazepam, Phenytoin
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22
Q

______ are the most potent inhibitors of gastric acid secretion → inhibit 90–98% of 24-hour acid secretion

A

Proton pump inhibitors are the most potent inhibitors of gastric acid secretion → inhibit 90–98% of 24-hour acid secretion

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23
Q

PPIs ____ bind and inhibit the ____ ATPase pump of gastric ____ cells

A

PPIs irreversibily bind and inhibit the H+-K+ ATPase pump of gastric parietal cells

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24
Q

PPIs suppress the final ____ pathway of gastric acid secretion

A

PPIs suppress the final common pathway of gastric acid secretion

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25
Q

describe the image

A

PPIs effectively suppress both basal and meal stimulated gastric acid production

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26
Q

list PPIs

A
  • Omeprazole
  • Esomeprazole
  • Lansoprazole
  • Rabeprazole
  • Pantoprazole
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27
Q

list the indications for PPIs

A
  • Patients who fail twice-daily H2RA therapy
  • Severe symptoms of GERD that impair quality of life
  • PUD
    • H. pylori eradication
    • NSAID associated ulcers
    • Prevention of peptic ulcer rebleeding
  • Gastrinoma
  • Nonulcer dyspepsia
  • Prophylaxis against stress-related gastritis
28
Q

PPI adverse effects

A
  • Vitamin B12 deficiency – d/t reduced pepsin function
  • Increased risk of CAP and C. difficile colitis
  • Hypomagnesemia
  • Osteopenia – possibly via reduced Ca2+ absorption or osteoclast inhibition
  • All PPIs carry an FDA-mandated warning of a possible increased risk of hip, spine, and wrist fractures
  • Diarrhea, abdominal pain and headache reported in less than 5% of patients
29
Q

____ and ____ inhibit CYP450 decreasing metabolism of which drugs?

A

Omeprazole and Cimitidine inhibit CYP450 decreasing metabolism of Warfarin, Diazepam, Phenytoin

30
Q

Clopidogrel is a prodrug that requires activation by the hepatic P450 _____ isoenzyme

A

Clopidogrel is a prodrug that requires activation by the hepatic P450 CYP2C19 isoenzyme

31
Q

list the drugs that inhibit CYP2C19 and their effect on clopidogrel

A

(LEO) Lansoprazole, Esomeprazole, Omeprazole inhibit CYP2C19

May reduce clopidogrel activation in some patients

32
Q

____ and ____ are preferred in persons taking clopidogrel

A

pantoprazoleor and rabeprazole are preferred in persons taking clopidogrel

33
Q

H. Pylori is a Gram ____ bacterium, contains ____ and _____ making it highly motile.
It causes inflammatory response, with increased risk of:

A

H. Pylori is a Gram negative bacterium, contains urease and flagella making it highly motile.
It causes inflammatory response, with increased risk of:

  • Peptic ulcer disease (esp. duodenal)
  • Gastritis
  • Gastric lymphoma
  • Gastric adenocarcinoma
34
Q

H. Pylori eradication triple therapy combines two ____ with a ____, resulting in <15% recurrence

A

H. Pylori eradication triple therapy combines two antibioticts with a PPI, resulting in <15% recurrence

35
Q

describe how PPIs promote eradication of H. pylori

A
  1. Direct antimicrobial properties
  2. Raising intragastric pH → lowers minimal inhibitory concentrations of antibiotics needed to clear the organism
36
Q

Triple therapy for ____ days - which drugs?

A

Triple therapy for 10-14 days - which drugs?

Clarithromycin + Amoxicillin + PPI

Clarithromycin + Metronidazole + PPI

37
Q

Quadruple therapy for ___ days - which drugs?

A

Quadruple therapy for 14 days

Bismuth Subsalicylate + Metronidazole + Tetracycline + PPI

38
Q

list the mucosal protective agents

A
  • Misoprostol
  • Sucralfate
  • Bismuth Subsalicylate
39
Q

Misoprostol is a ____ analog,
binds to EP3 receptor on parietal cells →

stimulates ___ pathway → decreasing _____ secretion

Stimulates ___ and ___ secretion.

Enhances mucosal ____.

A

Misoprostol is a PGE1 analog,
binds to EP3 receptor on parietal cells →

stimulates Gi pathway (decr. cAMP) → decreasing gastic acid secretion

Stimulates mucus and bicarbonate secretion.

Enhances mucosal blood flow.

40
Q

Misoprostol is approved for prevention of _______ ulcers in high-risk patients.

A

Misoprostol is approved for prevention of NSAID-induced ulcers in high-risk patients (NSAIDS block PGE1 production)

41
Q

Misoprostol AEs/contraindications

A
  • Diarrhea, abdominal pain and/or cramps, occur in 30% of patients
  • Contraindicated in pregnancy d/t abortifacient effects
42
Q

Sucralfate MOA

A
  • Sucralfate: salt of sucrose + sulfated aluminum hydroxide
  • Forms viscous paste that binds selectively to ulcers
  • (-)charged sucrose sulfate binds (+)charged proteins forming a physical barrier → restricting further caustic damage
  • Stimulates mucosal prostaglandin and bicarbonate secretion
43
Q

Sucralfate clinical use

A

Limited to the initial management of gastroesophageal reflux disease in pregnancy

44
Q

Bismuth subsalicylate (BSS) suppresses ____.

Does it have a neutralizing action on gastric acid?

A

Bismuth subsalicylate (BSS) suppresses H. pylori.

NO neutralizing action on gastric acid.

45
Q

Bismuth Subsalicylate clinical use

A
  • Quadruple antibiotic therapy of H. pylori-positive ulcers
  • Pepto-Bismol is widely used for dyspepsia and acute diarrhea
46
Q

Bismuth toxicity and contraindications

A
  • Rare
  • Metabolite bismuth sulfide causes harmless blackening of the stool → may be confused with gastrointestinal bleeding
  • BSS can cause salicylate toxicity in combination with other salicylate products
  • Contraindicated in patients with renal failure.
47
Q

Prokinetic agents MOA

Ideally should act ___ of ACh.

A
  • Enhance coordinated GI motility
  • Ideally should act “upstream” of ACh, at receptor sites on the enteric neuron itself, or higher
48
Q

Why are muscarinic (M1) receptor agonists not currently preferred for treating GI motility disorders?

A

Activated muscarinic (M1) receptors enhance contractions in a relatively uncoordinated fashion, producing little or no net propulsive activity.

Thus, bethanechol (cholinomimetic agent) and Neostigmine (ACh esterase inhibitor) are not currently preferred for treating GI motility disorders

49
Q

Erythromycin is an ____. It has ____ effects at the ___ receptor. Rapid down-reguation of this receptor leads to ______→ use is limited to short courses.

A

Erythromycin is an antibiotic/macrolide. It has agonistic effects at the motilin receptor. Rapid down-reguation of this receptor leads to early tolerance → use is limited to short courses.

50
Q

Best established indication for Erythromycin

A

Diabetic gastroparesis

51
Q

Describe Cisapride

A
  • 5-HT4 Agonist
  • 5-HT3 Antagonist
  • Direct smooth muscle stimulant
  • Was commonly used for gastroesophageal reflux disease and gastroparesis
  • No longer available in the U.S. because of its potential to induce serious and occasionally fatal cardiac ventricular arrhythmias
52
Q

describe Metoclopramide

A
  • 5-HT4 receptor agonist
  • Vagal and central 5-HT3 Antagonist
  • Dopamine (D2) receptor antagonist
  • Effects confined to upper digestive tract
    • Increases LES tone
    • Stimulates antral and small intestinal contractions
53
Q

Metoclopramide clinical indications

A
  • Gastroparesis
  • Anti-emetic
  • Previously used in GERD for symptomatic relief. Acid suppression therapy is far more efficacious/preferred.
54
Q

Metoclopramide AEs

A
  • Extrapyramidal effects d/t DA antagonism
    • MC in children/young adults, at higher doses
  • Galactorrhea → blocks inhibitory effect of dopamine on prolactin release. Rarely seen clinically.
55
Q

Molecular Targets of the Vomiting Reflex

A
56
Q

describe the 2 phases of Chemotherapy Induced Nausea and Vomiting (CINV)

A
  1. Acute phase - universally experienced (within 24 hours)
  2. Delayed phase - affects only some patients (days 2-5)
57
Q

list drugs to prevent CINV

A
  • Antimuscarinics: Scopolamine
  • H1 Antagonists: Diphenhydramine, Meclizine, Cyclizine
  • 5-HT3 Antagonists: ​Ondansetron, Granisetron
  • NK1 Antagonists: Aprepitant, Fosaprepitant
  • D2 Antagonists: Promethazine, Droperidol
  • Corticosteroids: Dexamethasone, Methylprednisolone
  • Benzodiazepines: Lorazepam, Alprazolam, Diazepam
  • Cannabinoids: Dronabinol
58
Q

describe Scopolamine

A
  • Antimuscarinic
  • Prevention & treatment of motion sickness
  • May have some activity in postoperative nausea and vomiting
  • Anticholinergic agents are NOT 1st-line DOC for CINV
59
Q

describe Diphenhydramine, Meclizine, and Cyclizine

A
  • H1 Antagonists for CINV
  • Act on vestibular afferents and brainstem
  • Useful for motion sickness and postoperative emesis
60
Q

describe Ondansetron and Granisetron

A
  • 5-HT3 Antagonists
  • Ondansetron = prototypical drug of this class
  • 5-HT3 receptors are present in several critical sites involved in emesis, including vagal afferents, the STN, CTZ and AP
61
Q

What is the DOC for prophylaxis against immediate CINV?

A

5-HT3 receptor antagonists

  • Also effective against hyperemesis gravidarum
  • Not very effective against:
    • Delayed CINV
    • Motion sickness
  • Well tolerated
62
Q

describe Aprepitant/Fosaprepitant

A
  • NK1 Antagonists
  • Fosaprepitant - Parenteral formulation
  • Antagonists of the NK1 receptors for substance P
  • Indicated for prophylaxis against delayed CINV, caused by moderate to highly emetogenic drugs
  • Given orally in combination with dexamethasone and a 5-HT3 receptor antagonist
63
Q

Which NK1 Antagonist undergoes extensive CYP3A4 metabolism? What are the affects of this?

A
  • Aprepitant undergoes extensive CYP3A4 metabolism
  • may affect the metabolism of warfarin and oral contraceptives
64
Q

describe Promethazine and Droperidol

A
  • D2 Antagonists
  • D2 receptor antagonism at the CTZ
  • Antihistaminic and anticholinergic properties effectively treat motion sickness
  • Not very effective in CINV
  • Potential for adverse extrapyramidal effects
65
Q

describe Lorazepam, Alprazolam, Diazepam

A
  • Benzodiazepines
  • No intrinsic antiemetic effects
  • Useful adjuncts d/t sedative, amnesic, and anti-anxiety effects → reduces anticipatory component of nausea & vomiting
  • Facilitate GABA-A action in the central nervous system by increasing the frequency of chloride channel opening
  • AE: CNS depression and dependence
66
Q

describe Dronabinol (Δ-9-tetrahydrocannabinol)

A
  • Naturally occurring cannabinoid
  • Synthesized chemically or extracted from marijuana plant, Cannabis sativa
  • Stimulates CB1 receptors in the brainstem
  • Prophylactic agent in patients receiving cancer chemotherapy, when other anti-emetic medications are not effective
67
Q

Dronabinol AEs

A
  • Marijuana-like “highs”
  • Prominent central sympathomimetic activity
    • Palpitations, tachycardia, vasodilation, hypotension
    • conjunctival injection (bloodshot eyes)
  • Paranoid reactions/ thinking abnormalities
  • Abrupt withdrawal of dronabinol → an abstinence syndrome (irritability, insomnia, and restlessness)
  • Great caution prescribing to persons with substance abuse Hx

Pharm (6 decks)

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