GI Drugs Flashcards
drugs used in acid-peptic diseases
Drugs that reduce intragastric acidity
- Proton Pump Inhibitors
- H2-Receptor Antagonists
- Antacids
Drugs that promote mucosal defense
- Sucralfate
- Prostaglandin Analogs
- Bismuth Compounds
GERD treatment goals
o Alleviate/eliminate sx o Decrease reflux frequency, recurrence & duration o Promote injured mucosal healing o Prevent complication development o Therapy target: -Increase lower esophageal sphincter (LES) pressure – you need the stomach to empty fast enough so that the acid doesn’t splash back up -Enhance esophageal acid clearance -Improve gastric emptying -Protect esophageal mucosa -Decrease refluxate acidity -Decrease gastric volume
GERD treatment phase I
o Lifestyle modifications
- Elevate the head of the bed – laying flat – no gravity to help them
- Stop smoking (decreases spontaneous esophageal sphincter relaxation) - Nicotine in any way decreases sphincter relaxation
- Avoid alcohol (increases amplitude of the lower esophageal sphincter, peristaltic waves and frequency of contraction)
- Avoid tight-fitting clothes
o Dietary changes
- Avoid irritating foods – different for everyone so you have to talk to the pt about what their trigger foods are
- Small meals and avoid eating within 3h before sleeping (decrease gastric volume)
- Weight reduction
o Avoid drugs that may worsen
o Patient-directed therapy with antacids and/or OTC H2-receptor antagonists
symptoms associated with GERD
-Belching
-Difficulty or pain when swallowing (Dysphagia)
-Waterbrash (sudden excess of saliva)
-Chest Pain
-Chronic sore throat
-Laryngitis
-Inflammation of the gums – dentists will sometimes recognize GERD due to these symptoms
-Erosion of the enamel of the teeth
-Chronic irritation in the throat
-Hoarseness in the morning
-A sour taste
-Bad breath
o 10-20% GERD prevalence in Western world
GERD factors worsening symptoms
o Foods
- Caminatives (peppermint, spearmint)
- Chocolate
- Coffee, cola, tea
- Fatty meal
- Garlic Onions
- Spicy foods
- Orange/tomato juice
o Medications
- Anticholinergics
- Barbiturates
- Benzodiazepines
- Caffeine
- Dihydropyridine calcium channel blockers
- Dopamine
- Estrogen – one of the most common symptoms of pregnancy
- Ethanol
- Isoproterenol
- Narcotics
- Nicotine
- Nitrates
- Progesterone
- Theophylline
- Alendronate
- Aspirin
- Iron
- NSAIDs
- Quinidine
- Potassium Chloride
GI tract and pregnancy
o When you are pregnant, your whole GI tract slows down!! ¼ of the speed to ensure absorption of the most nutrients as possible
o 3 reasons pregnant women get it: slowed GI, extra estrogen, pressure form baby
GERD treatment: phase II
o Acid-suppressing therapy
-H2 receptor antagonists
-Proton pump inhibitors (Start if present with more severe sx or with erosive esophagitis)
-Other: Pro-motility agents, sucralfate (rare)
o Maintenance therapy: 70 - 90% will relapse in 1 year after d/c
o Consider long term therapy
-Relapse
-Complications (Barrett’s esophagus, strictures, or hemorrhage)
o Use standard doses unless less-severe disease
o More severe - Higher doses in complicated sx, high-grade erosive esophagitis
o Barrett’s esophagus- normal stratified squamous epithelium replaced by abnormal columar epithelium
Zollinger-Ellison syndrome - treatment goals
o Gastrin-secreting tumors
o Locate and possibly reduce gastrinoma
o Surgical options
o Medical management
-PPI , H-2 antagonists are not curative, but limit complications.
o Condition in which there is increased production of gastrin sometimes caused by tumor in pancreas or small intestine
o NSAIDs block COX1 and therefore decrease prostaglandin synthesis – increase risk of ulcers
-Naproxen is worse for ulcers! You could go to a selective NSAID (Celebrex, etc. that are COX2 selective)
peptic ulcer disease - treatment
o Varies depending on etiology, initial or recurrent, complications
o Relieve pain, heal ulcer, prevent recurrence and reduce complications
o Eliminate/reduce irritants
-NSAIDs (If cannot discontinue administer with food or H2-receptor antagonist or PPI)
-Eradicate HP
o PPI’s provide more rapid symptom & faster ulcer healing
o 90% of PU caused by H.Pylori or NSAIDs !!!!
PUD - treatment
o NSAIDs
- Empirically treat with H2 blocker or PPI
- If NSAID is discontinued, uncomplicated ulcer heals with H2 blocker, PPI or sucralfate
- Larger ulcers require PPI or prolonged treatment
- PPI’s reduce ulcer incidence & complications in pts continuing aspirin or NSAIDs
- NSAID dose reduction, use acetaminophen or nonacetylated salicylates, relatively selective COX-2 inhibitors (nabumetone, etodolac, meloxicam, celecoxib)
o Prevent rebleeding
- High dose or continuous intravenous PPI infusion for 3-5 days reduces rebleeding
- Intragastric pH>6 enhances coagulation and platelet aggregation
Antacid - base 101
o NaHCO3 + HCl CO2 + NaCl
-CO2 is going to cause burping or farting – this is sometimes uncomfortable or embarrassing
o CaCO3 + HCl CO2 + CaCl
o Al(OH)3 + HCl H2O + AlCl3
o Mg(OH)2 + HCl H2O + MgCl2
o Simethicone (antiflatulant)
-Alters elasticity of mucus-coated bubbles, causing them to break
-Used often, but there are limited data to support effectiveness
-80mg po (chewed tablets) QID
consequences of PPIs instability
o PPIs formulation protects itself from stomach’s acidic pH by enteric coating
o Pantoprazole & Rabeprazole
-Coated tablets → they cannot be crushed
o Omeprazole, Esomeprazole & Lansoprazole
-Coated granules → they can be opened
o Weak antacids or alkaline juices may break the enteric coat
o Unlike antacid, PPI must be absorbed into blood stream first
o Need to take it before the largest meal
how are PPI’s are administered
-administered as inactive prodrugs. To protect the acid-labile prodrug from rapid destruction within the gastric lumen, oral products are formulated for delayed release as acid-resistant, enteric-coated capsules or tablets. After passing through the stomach into the alkaline intestinal lumen, the enteric coatings dissolve and the prodrug is absorbed. For children or patients with dysphagia or enteral feeding tubes, capsules may be opened and the microgranules mixed with apple or orange juice or mixed with soft foods (applesauce). Lansoprazole is also available as a tablet formulation that disintegrates in the mouth, or it may be mixed with water and administered via oral syringe or enteral tube. Omeprazole is also available as a powder formulation (cap or packet) that contains sodium bicarbonate (1100-1680 mg NaHCO3) to protect the naked (non-enteric-coated) drug from acid degradation. When administered on an empty stomach by mouth or enteral tube, this “immediate-release” suspension results in rapid omeprazole absorption (Tmax <30 minutes) and onset of acid inhibition.
24-hour intragastric acidity - mild to moderate GERD = H2
o If you have pt with active ulcer with H pylori or Zolinger Ellison, Barretts esophagus = PPI
o PPis are pretty flat except a little bump at night
o PPIs easily last 24 hrs – so if someone has one large meal and its dinner, then have them take the PPI before dinner and it should last until the next day
stress related mucosal damage (SRMD)
o Stress ulceration 1.5 to 8.5% of ICU patients, but up to 15% of patients not on prophylaxis.
o Ulceration in proximal regions of the stomach within hours of major trauma or serious illness
o Likely due to both:
-impaired mucosal protection (due to poor perfusion, uremic toxins, refluxed bile salts
-Hypersecretion of acid (gastrin stimulation of parietal cells
o Influence of H. Pylori infections?
o Prophylax in pts on tube feeds may increase mortality and HCAP w/o reducing GI bleeding
-DO NOT proph low risk pts
o Prophylaxis should be given to all patients with the following risk factors:
-Coagulopathy (Plts under 50, INR over 1.5, or PTT over 2x control)
-Mechanical vent over 48hrs
-h/o GI bleed in last year
-Traumatic brain/spinal injury
-Burn patients
-Two or more of the following: Sepsis, ICU stay over 1 week, Steroids over 250mg HCT, h/o GI bleed over 6 days
o if pts aren’t high risk, it can actually increase mortality!! DO NOT PROPHYLAX LOW RISK PTS!!!
