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S2B1: Pharmacology > Gastrointestinal Pharmacology > Flashcards

Gastrointestinal Pharmacology Flashcards

1
Q

What are the two causes of peptic ulcers? – Aggressive factors that contriubute to their developpment?

What are the body’s defense mechanisms against the development of peptic ulcers?

A
  • Causes
    • Helicobacter pylori
    • Long term use of NSAIDs (indomethacin and ibuprofen)
  • Aggressive factors
    • gastric acid & smoking (nicotine stimulates gastric acid)
  • Defense mechanisms
    • mucus
    • bicarbonate
    • blood flow
    • prostaglandins
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2
Q

Describe the control of gastric acid secretion.

A
  • When parasympathetic nervous system is activated (drink food/caffeine)
    • increases gastrin level – stimulates ECL cells to
      • release histamine – stimulates H2 receptor on parietal cells
        • increases intracellular cAMP level
          • increases activity of proton/K+ ATP pump,
            • which increases gastric acid (HCl) secretion
    • increases release of ACh, which acts on M3 receptor on parietal cells
      • increases intracellular Ca2+ level, which increases activity of proton/K+ ATP pump
        • which increases gastric acid (HCl) secretion
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3
Q

What are the 4 classes of drugs that can decrease gastic acidity?

A
  1. H+/K+- ATPase inhibitors
  2. H2 blockers
  3. Antacids (weak bases)
  4. Anticholinergics (not common b/c systemic adverse effects)
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4
Q

What are the PPIs & what is their mechanism of action?

A
  • Drugs
    • omeprazole (prilosec, rapine, zegerid)
    • Lansoprazole (prevacid)

protom pump inhibitors

  • react with H+/K+ ATPase to irreversibly inactivate the enzyme
    • lasts lifetime of the pump, so long-lasting
  • inhibit both fastign and meal stimulated secretion
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5
Q

Pharmacokinetics of PPIs?

A
  • Prodrugs
    • orally administered, absorbed in intestin & activated in parietal cells
    • slow onset of action
    • bioavailability is decreased by food
      • except dexlansoprazole
    • Rapid first-pass hepatic metabolism
      • CYP2C19
      • CYP3A4
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6
Q

Clinical uses of PPIs?

A
  • Peptic ulcer disease: first-line drugs & most widely used
  • sever symptomatic GERD
  • nonulcer dyspepsia
  • Prevention of stress-related mucosal bleeding
  • gastric acid hypersecretion: gastrinoma
  • Prevent NSAIDS-induced GI side effects
    • ie. patients with arthritis
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7
Q

Adverse effects of PPIs?

A
  • well tolerated & relatively safe
    • nausea, diarrhea, abdominal pain
  • Long-term use
    • increase Clostridioides difficle-associated diarrhea
      • b/c increased gastric pH
    • may reduce plasma Vitamin B12, non-heme iorn, Ca2+, Mg2+ levels
      • b/c the reduced release of these components from food due to the increased gastic pH
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8
Q

drug-drug interaction PPIs?

A
  • drugs that the bioavailability is affected by intragastric acidity
    • itraconazole
    • digoxin
  • Esomerprazole and omeprazole: CYP2C19 inhibitors
    • interact with
      • phenytoin
      • diazepam
      • theophyline
      • clopidogrel
    • dosage adjustment
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9
Q

What are the H2 Histamine receptor antagonists and what is their mechanism of action?

A
  • Drugs
    • Cimetidine (tagamet)
    • Famotidine (pepcid)
    • ranitidine (Zantac)
  • mechanism of Action
    • competitively and selectively bind to H2 receptors, therefore reduce histamine-induced acid
    • therefore, do not COMPLETELY block gastric acid secretion
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10
Q

Clinical uses H2 receptor antagonists?

A
  • Peptic ulcer disease: first-line drugs & most widely used
  • sever symptomatic GERD
  • nonulcer dyspepsia
  • Prevention of stress-related mucosal bleeding
  • gastric acid hypersecretion: gastrinoma
  • Prevent NSAIDS-induced GI side effects
  • ie. patients with arthritis
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11
Q

Adverse effects H2 receptor antagonist?

A
  • extremely safe. Tolerance develops
    • cimetidine: ginds to dihydrotestosterone receptors – exaggerated estrogen effects
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12
Q

Drug-drug interaction of H2 receptor antagonists?

A
  • interact with drugs metabolized by
    • CYP1A2
    • CYP2D6 and/or
    • CYP3A4 (azole antifungal agents)
  • affect inhibit first-pass metabolism of ethanol
    • except famotidine
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13
Q

What is the mechanism of action of antacids?

A
  • neutralize gastric acid
  • Mg2+, Al3+, Na+, and Ca2+ salts are the most common
  • very rapid, but short duration of action
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14
Q

clinical uses of antacids?

A

short-term relief of symptoms, used as-needed basis

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15
Q

adverse effects of antacids?

A
  • constipation (aluminum)
  • diarrhea (magnesium)
  • altered electrolyte balance
  • if you combine both calcium & magnesium can reduce both constipation & diarrhea
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16
Q

drug-drug interactions of antacids?

A
  • affects absorption of some antibiotics
    • tetracyclines & fluroquinolones
    • separate administration time by several hours
17
Q

Antibiotics used to cur H. pylori infection-induced peptic ulcer

A
  • First line
    • clarithromycin
    • amoxicillin
    • tetracycline
  • second line
    • Metronidazole
      • if allergic to penicillin
    • Refabutin
      • if clarithromycin or metronidazole resistance
18
Q

What is the drug name & mechanism of action for colloidal bismuth compounds?

A
  • name
    • bismuth subsalicylate (pepto-bismol)
  • mechanism of action
    • coat ulcer and erosions
    • stimulate the secretion of prostaglandin, mucus, and bicarbonate
    • antimicrobial effects: bind to bacteria and enterotoxins
    • reduced stool frequencey and liquidity
19
Q

Clinical uses of Bismuth compounds?

A
  • nonprescription: treat dyspepsia dn prevent traveler’s diarrhea
  • combined with PPI and antibiotics: H. pylori infection-caused peptic ulcer
20
Q

Adverse effects & contraindications for bismuth compounds?

A
  • adverse effects
    • black tongue and stool
  • contraindication
    • renal insufficiency and allergies to salicylates
21
Q

Sucralfate mechanism of action?

A
  • pepsin inhibitor
  • activated by acid – treating w/ antacid will decrease efficiency
  • Mechanism of action (protect mucosa)
    • physical barrier
    • inhibit pepsin mediated hydrolysis of mucosal protein
    • stimulates mucosal prostaglandin and bicarbonate secretion
22
Q

Clinical uses of sucralfate?

A
  • prophylaxis of stress gastritis
  • peptic ulcer
  • ulcers not caused by acid: oral mucositits and bile reflux gastropathy
23
Q

Adverse effects & drug-drug interactions of sucralfate?

A
  • adverse effects
    • may develop constipation due to the aluminum salt
  • drug-drug interaction
    • may reduce the absorption of some oral medications
    • time-lapse is important
24
Q

Draw this

A
25
Q

What is the 3 step treatmetn strategy for H. pylori peptic ulcer?

Provide example of the triple therapy.

Provide example of quadruple therapy.

A
  1. elimate the bacteria (antibiotics)
  2. reduce stomach acid (protom pump inhibitor)
  3. protect the mucus membrane (bismuth subsalicylate)
  • Triple therapy
    • PPI-CA: PPI + clarithromycin + amoxicillin
    • PPI-CM: PPI + clarithromycin + metronidazole
      • penicillin allergy
    • PPI + amoxicillin + rifabutin
      • clarithromycin or metronidazole resistance
  • Quadruple therapy
    • Bismuth-based quadruple therapy
      • bismuth subsalicylate + mtronidazole + tetracycline + a PPI
    • Clarithromycin-based quadruple therapy
      • amoxicillin + clarithromycin + metronidazole + a PPI
26
Q

What are the therapeutic strategies to treating inflammaoryt bowel disease?

What are the two common inflammatory bowel diseases?

A
  • Therapeutic strategies
    • inhibit the inflammatory responses
    • suppress immune responses
  • Inflammatory boewl disease
    1. Ulcerative colitis (UC)
    2. Crohn’s disease (CD)
27
Q

What is the inflammatory supressor? What is it ised to treat?

A

Inflammatory bowel

  • 5-Aminosalicylates (5-ASA, mesalamine:
    • Sulfasalazine: 5-ASA-AZO bond-sulfapyridine
      • sulfapyridine can be absorband & causing adverse effects
    • Olsalazine: 5-ASA-AZO bond-5-ASA
    • Balsalazie: 5-ASA-AZO bound-inert compound
28
Q

5-ASA mechanism of action?

A
  • not fully understood
  • Thought to inhibit the following:
    • IL-1 and TNF-alpha expression
    • lipoxygenase pathway
    • NG-kB
    • reactive oxygen species
29
Q

Clinical uses of 5-Aminosalicylates?

A
  • induce and maintain remissionof mild or moderate ulcerative colitis (inflammatory bowel disease)
  • Rheumatoid arthritis (sulfasalazine)
30
Q

Adverse effects & drug-drug interactions of 5-Aminosalicylates?

A
  • Adverse Effects
    • sulfasalazine
      • more adverse effects
    • others: well tolerated
      • dyspepsia (indegestion)
      • skin rash
      • headache
      • abdominal pain
      • rare but serious: nephrotoxicity
  • Drug-drug interactions
    • fomulations with pH sensitive enteric coatings shouldn ot be co-administerd with anti-acids
    • if co-administered with anti-acid drugs, they will not make it to the intestines
31
Q

What the glucocorticoid/corticosteroids? What are they used to treat?

A

Used to treat inflammtory bowel disease

  • prednisone and prednisolone: oral
  • Budesonide
    • oral
    • synthetic analogue of prednisolone
    • extensive first-pass metabolism by CYP3A4 – low bioavailability – les change to cause systemic adverse effects
  • Hydrocortisone: enemas, foam or suppositories
32
Q

Glucocorticoid/corticosteroids mechanism of action?

A
  • Overview
    • produced by adrenal glands
    • only free form will enter into the cells
      • bind to specific receptors
      • will dimerize into the nucleus
      • bind to glucocorticoid response element in the gene
        • effect gene expression & protein expression
          • alter cellular function
  • MOA
    • inhibit expression inflammatory mediators
    • increase expression of antiinflammatory mediators
33
Q

Clincal uses of glucocorticoid/corticosteroids?

A
  • Budesonide
    • induce remission in mild adn moderate IBD
  • Prednisone and prednisolone
    • induce remission and control acute moderate to severe active IBD
    • more potent than 5-ASAs
34
Q

Adverse effects and drug-drug interactions with glucocorticoid/corticosteroids?

A
  • Adverse Effects
    • prolonged use (except budesonide) can cause lots of adverse effects adn the drugs have to be tapered gradually when discontinuing
      • mood changes, fluid retention, increased appetite and glucose level
      • increase chances of infection, peptic ulcers, osteoporosis, glaucoma, and cataract
      • High dose:
        • hypothalamic-pituitaty-adrenal axis suppression
        • temorarily show growth rate in children
  • Drug-drug ineractions
    • budesonide interacts wtih CYP3A4

S2B1: Pharmacology (5 decks)

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