GI/GU Flashcards
(52 cards)
medication classes that can cause GERD (7)
Anticholonergics ASA / NSAID Barbiturates BZDs Bisphosphonates CCBs Electrolytes (Fe, K+)
How do anticholinergics cause GERD?
anti-cholingergics = anti- SLUD, so causes constipation, slowing gastric emptying = reflux
How do ASA / NSAIDs cause GERD?
inhibit prostaglandin secretion. prostaglandin helps form protective layer in stomach. Without it, ulcers and bleeding may occur.
How do barbiturates cause GERD?
slow gastric emptying
How do BZDs cause GERD?
causes less LES functioning
How do bisphosphonates cause GERD?
they can cause problem directly on the esophagus
How do CCBs cause GERD?
Ca causes constipation, slowing system down, delaying gastric emptying
How do electrolytes cause GERD?
a lot of N/V and GI upset with these medications
TYPICAL symptoms of GERD (and what does “typical” mean?) [4]
Typical symptoms are those that are subjective and patient-reported, so a clinician may not observe them themselves.
Typical symptoms of GERD: heartburn/pyrosis
regurgitation
hypersalivation
belching
OTHER symptoms of GERD [4]
WHEN: water brash, hiccups, early satiety, N/V
ALARM SIGNS of GERD (and what does “alarm signs” mean?) [6]
Alarming signs: severe, hospitalize
Alarming signs of GERD: continual pain dysphagia/odynophagia coffee-ground emesis melena stool unexplained weight loss anemia
ATYPICAL symptoms of GERD (and what does “atypical” mean?) [6]
atypical symptoms- are signs/symptoms that are a little more alarming, but not quite an alarm sign
Atypical symptoms of GERD: non-cardiac chest pain chronic cough vocal cord irritation hoarseness pharyngitis dental erosions
signs vs symptoms
signs- measurable (lab values, tests), objective; something a healthcare provider can measure, observe and/or document
symptoms- subjective to the patient (ex: pain) willing to or remembering their experience
Modifications for GERD
avoid trigger foods or take TUMS or Pepcid after eating
avoid having large meals; causes irritation/preventing closing of the LES
don’t eat before you sleep
sometimes pill gets lodged in back of throat; drink with water
stop smoking
limit alcohol intake
lose weight
elevate head of bed by 6-8 inches so food goes down via gravity
tight-fitting clothes restrict and push contents back up
PUD
PUD = peptic ulcer disease; ulcerative disorder
the ulcers can be duodenal or in the upper GI tract.
Once an ulcer forms, it’s kind of like a pothole; these erosions keep getting bigger as bile acids settle there- can spread to muscularis mucosa
clinical presentation: duodenal ulcer vs gastric ulcer
duodenal ulcers typically present with epigastric pain, food will RELIEVE pain of the ulcer, H. pylori known to cause
gastric ulcers; you may see epigastric pain, but more commonly see N/V, food will WORSEN the pain because it stimulates even more bile acid formation, NSAID like aspirin cause (inhibit protective production of prostaglandins, sit on stomach)
PUD vs GERD
PUD = ulcers GERD = disfunction of LES, reflux of food into esophagus
PUD can present similar to GERD but are different
Contributory factors: GERD
aspirin worry/stress caffeine spicy foods all tobacco use (especially smoking)
Top 200 GERD / PUD agents
PPIs and H2RAs
PPIs vs H2RAs in treatment of GERD or PUD
- both highly effective
- both gastric anti-secretory
- PPIs work better to prevent acid production, but in general
- H2RAs work after acid is produced and block histamine 2 receptors
PPIs (Top 200 name brand and generic)
- omeprazole (Prilosec)
- pantoprazole (Protonix)
- lansoprazole (Prevacid)
- esomeprazole (Nexium)
- dexlansoprazole (Dexilant)
H2RA (Top 200 name brand and generic)
ranitidine (Zantac)
famotidine (Pepcid)
H2RA use
- PUD, mild-moderate GERD
- MOA: inhibit gastric parietal cell H2 receptors, thus suppressing basal and post-prandial acid secretions.
- Absorbed in the intestine; don’t directly act directly in stomach- go though intestines and body and then have their effect.
- Generally safe and well-tolerated (HA, somnolence, dizziness; may take without regard to meals
- IV and PO
- Tachphylaxis may occur
PPI
PUD, mild-moderate GERD
MOA: inhibiting proton pump (H/K ATPase), preventing acid from even being produced, so that’s why it’s effect is a little better than the H2RAs
This drug is not going to be active locally initially, must be absorbed, go to liver, and do its work there. prodrugs= not activated until absorbed, goes to liver, converted to active form, circulated back to stomach and inhibits those proton pumps
CYP 2C19 is the enzyme that converts it to active form
Well tolerated (HA, diarrhea, abdominal pain)
Consequences:
- Lower Ca and B12 absorption
- increased risk of community acquired pneumonia and CDAD
