Medications for the GI tract

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  1. Antacids
    alkaline compounds that neutralizes acid in the stomach and increases the pH

    Clinical indicators (CI)- PUD, esophagitis (synphiter not working back up acid)(symptomatic relief)

    • MOA- react with the gastric acid to produce neutralize salts of low acid
    • - decreases the action of pepsin (pepsin increase HCL acid)
    • - increases production of prostagladins
    • - increase bicarbonate production

    dont heal ulcer but creates an enviorment so ulcer can heal
  2. Pepsin
    production HCL acid

    • pH> 4 reduces the HCL acid
    • pH between 2-4 (raising acid)
  3. Prostaglandins
    role in the stomach

    have a protective role in the tummy

    decrease acid level

    increase blood flow (to promote healing of ulcer)

    increase the cytoprotective membrane

    ulcer- reduces acid so it doesn't destroy the tissue), increase blood flow to promote healing, cytomembrane is increase to increase bicarbonate to create a more base enviroment
  4. Antacids (S/E)
    related to the agent/classification with nursing implication

    • Mg- diarrehea (loose stool)
    • Al: constipation
    • switch back and forth if needed for long term therapy
    • calcium carbonate (tums)- constipation/belching
    • Na bicarbonate (be careful with pt with htn and cardiac issue)- belching, flatus alkazer
  5. Antacid (nursing implication)
    • rapid onset
    • liquid is more effective than tablets
    • on an empty stomach it is 20-40 mins duration
    • with food it last longer
    • follow this with H2O (because u want to get it into the stomach unless pt have esophagitis than u want it to stay there)
    • careful regarding drug interaction (ph)
    • monitor Na and K levels (cardiac pt)
  6. H2 receptors antagonist
    H2 blockers histamine blockers

    ex- Zantac, pepcid (prevent ulcer)

    CI gastric and duodenal ulcers, increase ulcer healing rates, stress ulcers (change in the immune system) constant flight and fight (blood going to major organs), reflux esophagitis, aspiration pnuemonia (bed rest, dyphasia, cant follow instruction acid in the lungs), GI bleed (if u have a bleeding site and add acid to it it will bleed more, so u have to stop this

    • MOA- blocking of H2 receptors in the parietak cells of the stomach 
    • decreases acid production by 50-80%
    • selective for H2 receptors ONLY
  7. H1 receptors
    they work as anti histimine

    found in the upper respiratory tract- skin, bronchi, nose,

    • Competitive
    • Histamine wants to bind to H2 receptor creates increase of HCL acid. selective for only H2 cell
  8. H2 S/e and NI
    • well tolerated, mild
    • in elderly may have confusion with IV agents 

    NI usually works within an hour, can last for 6-8

    be aware of drug interaction. Antacid will decrease absorption(prevent H2 receptor from being active). smoking will decrease effectiveness
  9. Proton Pump Inihibitor (PPI)
    Most effective at reducing gastric acid secretion (anti ulcer agent)

    ex- Prilosec, Prevacid, Protonix

    CI- severe GI reflux, duodenal ulcers, hypersecretory disorders (secretory increase HCL), antibacterial effect on reducing H. pylori (bacteria found in the gut and could form peptic ulcer disease). 

    a single dose can decrease acid production by 90% in a 24 hour period of time. 

    effects can last up to 72 hours
  10. PPI (proton pump inhibitor) MOA
    • block the H-K AtPase pump (energy pump)
    • this is the last step of acid production 

    it blocks the H from getting into the cell therefore you can make HCL.
  11. PPI (proton pump inhibitor) S/e NI
    • S/E
    • less than 1%
    • headache, diarrehea, back pain, fracture (in menopausal women), colitis

    NI- be aware of drug interaction because it can impair metabolism of other drugs because it competes metabolic pathway. This drug also reduces acid so if u give a drug that likes acid it would decrease its use. 

    • do not crush
    • u can dissolve it in a weak acid solution
    • administer on an empty stomach
  12. Mucosal Protective Agents
    Cytoprotective agent

    Ex. carafate (locate)

    CI- gastric ulcers (protects mucosal barrier against acid), promotes healing
  13. Mucosal Protective agent MOA
    carafate (cytoprotective agent)

    local effect

    reacts with HCL acid to form a paste like substance that adheres to the gastric mucosa 

    creates barriers

    doesn't heal ulcers but promotes an enviroment for healing 

    last for 6-8 hours
  14. Mucosal protective agent S/e NI
    S/e Mild constipation

    • NI: best on an empty stomach b.c u need the acid to create the paste
    • drug interaction with antacid 
    • increase fluids to prevent constipation
    • carafate slurry- huge tablet so this can be dissolved in 30ml of water and it would be just as effective
  15. Gastric Stimulant 
    Pro Kinetic Agent
    • positive mobility agents
    • agents that is used to increase peristalsis and gastric emptying. also, anti emetic use

    Ex- reglan 

    CI- GERD, diabetic gastroparesis (delayed emptying), prevention of nausea
  16. Pro Kinetic (MOA) positive energy
    • Not clear
    • sensitizes tissues to Ach. cholinergic effect on upper gi tract. 

    increase ach. chlin to increase perstalisis (parasympathetic effect)

    • increases gastric perstalsis
    • increased tone of the lower esopaheal sphincter
    • increase gastric contractions
    • relaxes the pyloric sphcinter 

    anti emetic- blocks dopamine at CTZ (chemo receptor trigger zone in the brain)
  17. Pro Kinetic (S/E)
    CNS- drowiness, dizziness, headache, depression, confusion, hallucinations

    • EPS (extrapyramidal symptoms- controls voluntary movements, coordination- u need dopamine)- not coordinated, acute dystonia (muscle pain), Parkinsonism (mimics parkinson dx)
    • symptoms: shuffling, gait, ridigity
    • akathesia- motor restlessness (blocking dopamine) (usually occur 24-48 after the dosage more common with higher doses)
  18. Pro Kinetic NI
    • best 30 mins before a meal- want food to move along
    • IV reglan: infusion over 15 mins

    • assess for safety risk 
    • assess EPS and treat
    •   withhold the dosage and notify MD
    •   assess safety
    •   admin benadryl or cogentin (antedote- to reverse symptoms) to increase dopamine

    ach. cholene inverse relationship with dopamine
  19. Antiemetics
    SSR Antagonists (selective Serotonin Receptor Antagonist)


  20. Control of Vomiting
    • direct stimulation of vomiting from the vomiting center- comes from Cerebral cortex or the inner ear
    • we can vomit two ways: something that directly stimulates the vomiting center (from the brain or inner ear) or indirectly- CTZ which then stimulates VC (from the stomach and meds)

  21. SSR Antagonist (anti emetic)
    Ex- Zofran

    CI: to relieve nausea and vomiting

    MOA: blocks serotonin receptors in the CTZ and vagal nerves in the upper GI (indirect)

    extremely highly effective
  22. SSR S/e NI
    • S/E headache, diarrehea, malaise, mild, 
    • less likely EPS, sedation


    Drug interaction (P450 enzymes path)

    • competing for one pathway
    • so if there are other drugs competing for that pathway who ever has more wins. so it can be bumped out and not effective

    admins over 15 mins.
  23. Phenohiazides
    ex Phenergan, compazine

    CI: relieve nausea and vomiting

    MOA: blocks the action of dopamine on CTZ and GI tract (indirect method)
  24. Phenothiazides SE NI
    SE- hypotension, blurred vision, dizziness EPS

    • NI: safety
    • administered with food for gi interaction
    • safety EPS (admins benadryl congentin)
  25. Adjunct agent for controlling nausea

  26. Anticholinergics
    ex: antivert, benadryl

    CI- to relieve nausea, vomiting, motion sickness, vertigo 

    MOA blocks the action of achcholene on the vc, blocks the action of histimine on the inner ear (direct) block stimulation of the VC
  27. anticholinergics SE NI
    SE sedation (benadryl), anticholinergics effects cause- dry mouth, blurred vision, decrease sweating therefore increase temp, constipation, confusion

    • NI
    • safety CNS
    • interventions to decrease dry mouth and constipation
  28. Drugs for motion sickness
    Scopolamine (anticholinergic)
    • place this behind ear
    • prevents and treats motion sickness
    • inhibits Ach and decreases neuronal transmission
    • SE: mild antichol. 
    • apply patch 4 hrs before travel and last for 3 days waterproof

    be careful with withdrawl can make u sick.
  29. Motion sickness 
    • Prevents and treat nausea and vomiting, dizziness, and vertigo with motion
    • inhibits vestibular stimulation (inner ear)
    • SE- mild, drowsiness, dry mouth, photosensitivity (extra/ sun burn)
    • administer at least 30 mins before exposure  works best for 1-2 hrs
  30. drugs for Inflammatory Bowel Disease
    5 ASA Preparations

    ex- Mesalamine

    CI to treat mild or moderate IBD (inflammation in the intestine- increase stool, abd pain and cramping)
  31. Mesalamine (IBD) MOA SE NI
    • MOA- blocks cyclooxygenase (enzyme needed to convert pre cursor to prostagladins) and inhibits prostagladin (decreases pain and inflamm) production in the colon suppresses migration of inflammatory cells 
    • has local effect
    • SE: headache***, fever, rash, arthralgia, anemia, photosentivity 

    NI allergy to aspirin, assess CBC (because of anemia), BUN and creatinine
  32. Sulfasaizine
    CI: IBD ulcerative colitis

    it is a combination drug of mesalamine and sulfapyridine ( prevents mesalamine from being absorbed and execreted so it can stay in the intestine)

    • SE allergy to sulfa
    • turns the urine bright orange to yellow

    heartburn, gi s/s loss of apetite
  33. Other drus to treat IBD

Card Set:
Medications for the GI tract
2014-05-24 01:48:08

nursing student yey
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