GI system management Flashcards
Oral stage of swallowing
- can be initiated voluntarily or involuntarily
- food bolus formed and propelled backward toward pharynx
Pharyngeal stage of swallowing
- complex involuntary event activated by swallowing center
- swallowing centers stimulated, soft palate pulled upward, vocal cords approximated, epiglottis swings back, UES relaxes
Esophageal stage of swallowing
- food moves down esophagus via primary peristalsis over 8-10 secs
- secondary peristalsis occurs if food is still in esophagus after primary wave
- LES is relaxed
4 phases of proton pump secretion
- Basal (Interdigestive)
- Cephalic
- Gastric
- Intestinal
Basal phase of secretion
- occurs at night
- <30% max acid output
- controlled via Ach and histamine
Cephalic phase of secretion
- waking up in AM
- emotional/sensory stimuli produce excitation of vagal fibers
- vagal (parasympathetic) stim of parietal cells and antral G cells to produce H+ and peristalsis
Gastric phase of secretion
- food enters stomach
- intragastric buffering enhances secretion by maintaining less acidic pH
Intestinal phase of secretion
- food in intestine releases inhibitory factors
- <10% max acid output
Management of diarrhea
- Motility inhibitors
- Bulk formers
- Probiotics
Motility inhibitors
- Bismuth subsalicylate (Peptobismal)
- Diphenoxylate HCl with atropine (Lomotil)
- Loperamide (Imodium)
- Opium tincture
- Paregoric
Mechanism of action of motility inhibitors
-inhibit Ach receptors (parasympathetic) to slow GI motility by promoting water absorption in large bowl
Side effects of motility inhibitors
- Anticholinergic- dry mouth, urinary retention, blurred vision, tachycardia
- CNS- drowsiness, HA
Calcium polycarbophil (Fibercon)
- bulk former
- absorbs water in large bowel
- produces gel-like stool
Probiotics
- helpful for chronic diarrhea
- enhances microbial growth to inhibit harmful bacteria and promotes water reabsorption
- Culturelle
Managing Nausea/Vomiting
- CTZ suppressors
- H1 receptor antagonists
- Metoclopramide
- Dronabinol
Mechanism of action of CTZ suppressors
- most powerful antiemetic
- blocks postsynaptic dopamine receptors in chemoreceptor trigger zone (CTZ)
Mechanism of action of H1 receptor antagonists
- antihistamines that cross the BBB
- mechanism not well known
- produces anticholinergic effects
Metoclopramide
- antiemetic
- accelerate GI motility - promotes gastric emptying
- decreases N/V d/t GI overdistention
CTZ suppressors
- antiemetics
- Benzquinamide HCl
- Bulizine HCl
- Chlorpromazine
- Diphenidol
- Droperidol
- Prochlorperazine (Compazine)
- Thiethylperazine
- Trimethobenzamide HCl
- Ondansetron HCl (Zofran)
H1 receptor antagonists
- antiemetics
- Cyclizine
- Dimenhydrinate
- Diphenhydramine HCl
- Hydroxyzine
- Meclizine
Side effects of CTZ suppressors
- CNS depression (foggy, tired)
- hypotension
- resp. depression
- anticholinergic
- extrapyramidal effects (rare)
Medications for peptic ulcer disease
Antibiotics Bismuth subsalicylate PPI H2 receptor antagonist Sucralfate Prostaglandin E analog- Misoprostol
Antibiotics used for peptic ulcer disease
- Metronidazole
- Clarithromycin
- Tetracycline
- Amoxicillin
- Levofloxacin
Mechanism of action of proton pump inhibitors
inhibits proton pump to decrease H+ ions => decreases gastric acidity => increased pH promotes gastric healing
Proton pump inhibitors
Omeprazole (Prilosec) Lansoprazol (Prevacid) Rabeprazol (Aciphex) Pantoprazol (Protonix) Esomeprazole (Nexium) Dexlansoprazole (Dexilant)
Mechanism of action of H2 receptor antagonists
-inhibits binding of histamine at receptors in parietal cells => decreased pumping of H+ ions from parietal cells into gut => decreased acid irritation
H2 receptor antagonists
Cimetidine (Tagamet)
Famotidine (Pepcid)
Nizatidine (Axid)
Ranitidine (Zantac)
Side effects of H2 receptor antagonists
- dizziness, drowsiness, confusion
- abd discomfort, diarrhea
- overall well tolerated
What drug interactions are notable for H2 receptor antagonists
Antacids- decrease absorption
What labs can be effected by H2 receptor antagonists
Prolonged PT
Thrombocytopenia
Neutropenia
Sucralfate
- mucosal protective agent
- forms paste-like substance that adheres to damaged mucosa to protect from acid/irritants
- can alter absorption of other drugs- take 1-2 hrs from other drugs
- take several times a day
- shown to decrease risk of aspiration pneumonia since it does not change pH of gut
Misoprosol
- Protaglandin E analog
- replaces protective prostaglandins that are inhibited by NSAIDs => inhibits GI mucosal breakdown
- Side effects- diarrhea, HA
Management of H. pylori PUD
Combo of 2 abx and 1 acid suppressor (PPI or H2) x 14 days (triple, quadruple, sequential, or salvage regimens)
Triple drug regimen for H. Pylori
PPI + Clarithromycin + Amoxicillin or Flagyl x 10-14 days (80% success rate)
Quadruple drug regimen for H. Pylori
PPI + bismuth + metronidazole + tetracycline x 14 days
- for pts allergic to PCN or taking macrolides
Sequential regimen for H. Pylori
- may be more effective than triple therapy
- consider if pts recently on clarithromycin or metronidazole
- PPI + amox x 5 days, then PPI + clarithromycin + tinidazole x 5 days
Salvage therapy for H. Pylori
- for when initial treatment didn’t work
- use quadruple therapy if not already used
- PPI + amox +levofloxacin x 10 days
What patients are at high risk for peptic ulcers
- prior hx of ulcers or GI bleed
- taking high dose NSAID
- taking corticosteroids or anticoagulant
What prophylaxis is given to patient at risk for peptic ulcers
- COX2 NSAID with PPI (high risk)
- nonselective NSAID with PPI (moderate risk)
Management of duodenal ulcers
*more common Sucralfate QID or PPI QD x 4 wks or H2 receptor blocker QHS x 6 wks
Management of gastric ulcers
*more concerning, complicated
H2 receptor blocker BID x 8-12 wks
or
PPI BID x 6-8 wks
Regimen to prevent NSAID ulcer relapse
- COX2 NSAID with PPI once daily
- COX2 NSAID with misoprostol TID or QID
Management of GERD
PPI
- give in AM, 30-60 min prior to breakfast
- can do second dose prior to dinner
What medications can be used for both forms of IBS
- bulk-formers- Psyllium (Metamucil) and Methylcellulose (Citrucel)
- TCAs and SSRIs
Management of IBS-C
- 5HT4 agonists (not available in US)
- Polyethylene glycol (Miralax)
- Lubiprostone (Amitiza)
- Linaclotide (Linzess)
- Tenapanor (Ibsrela)
Lubiprostone (Amitiza)
- selective chloride channel activator
- increases fluid secretion into sm bowel => stim. GI motility
- side effect- benign chest tightness/SOB, resolves within 3hrs of admin
Linaclotide (Linzess)
- Guanylate cyclase-C agonist
- increases fluid secreation into gut by chloride and HCO3 channel activation
- decreases activation of pain-sensitive nerves
- primary adverse effect- diarrhea
Tenapanor (Ibsrela)
- very recently approved
- Na/H+ exchanger
- inhibits Na absorption to increase H2O in bowel => increases transit time and soften stool
Management of IBS-D
Eluxadoline (Viberzi) Probiotics Antidiarrheals Rifaximin (Xifaxin) Alosetron (Lotronex) Loperamide TCAs (2nd or 3rd line)
Eluxadoline (Viberzi)
- for IBS-D
- mu and kappa receptor agonist => analgesia
- delta receptor antagonist => decrease motility
- not for patient with: alcohol abuse, GI motility issues, or chronic/severe constipation
Alosetron (Lotronex
- for IBS-D
- 5HT3 recept. antagonist
- may cause ischemic colitis- black box warning: prescribers must be enrolled and patient has to sign agreement
Management of inflammatory bowel disease (IBD)
- monoclonal antibodies (TNF-alpha blockers)
- Mesalamine-5-ASA
Infliximab (Remicade)
Adalimumab (Humira)
Certolizumab (Cimzia)
- IBD (mod-severe)
- monoclonal antibodies that block receptors for TNF-alpha, a key inflammatory mediator
- trend is now to use earlier in therapy
- black box warning- risk for infections like TB
Mesalamine-5-ASA
- IBD
- decreases inflammation
- Pentasa, Rowasa, Asacol
Naloxagel (Movantik)
for Opioid-Induced Constipation
Methylnaltrexone (Relistor)
for Opioid-Induced Constipation
-SQ injection daily
PAMORA
for Opioid-Induced Constipation
