Med classes GI- Quiz 2 Flashcards
What are the 2 main causes of peptic ulcer disease?
- H. Pylori (H2 blockers)
- NSAIDs (PPI’s)
(Also, Increased production of HCl acid and inadequate mucosal defenses against gastric acid may contribute)
What is treatment for PUD aimed at?
- Clearing H. Pylori
- Reducing gastric acid
- Agents that protect the
gastric tissues from damage
How is H. Pylori diagnosed/ treated?
Diagnosed:
1. EGD or serology
2. Fecal antigen
3. Urea breath tests (patient cant have antacids, PPI, or H2 for 14 days prior) WHY DO I FEEL LIKE THIS IS A TEST ?
Treated:
-Combo of antimicrobials and acid suppressors (usually have low recurrence rate)
GI Antimicrobials Used for PUD
-Amoxicillin
* Bismuth
* Clarithromycin
* Metronidazole
* Tetracycline
What is the regimen of choice for PUD?
-Quadruple therapy with Pepto-Bismol, Flagyl, Tetracycline + PPI
(Second option is Triple therapy with PPI, Amoxicillin and Biaxin for those w/o recent use of macrolides)
H2 Blockers
-“Tidine’s”
-MOA: Act selectively on H2 receptors in the stomach, without effecting H1 receptors — they reduce the secretion of gastric acid
-Uses: PUD/ heartburn (takes longer to work but lasts longer than antacid)
Pharm: Distribute widely across body (including placenta/breast milk)
Half life: ½ life of these drugs are prolonged in renal disease—
dosage adjustments are needed
-ADE’s: Confusion in elderly
Cimetidine= gynecomastia/ galactorrhea
-Ex. Cimetidine, Famotidine, Nizatidine, and Ranitidine (removed from market d/t being carcinogenic)
-NOTE* Cimetidine is PROTOTYPE
for this family but rarely used today d/t ADE’S (inhibits many CYP 450 isoenzymes)*
What is considered first line treatment for GERD?
-PPI’s (esp those with severe/ frequent heartburn)
H+/K+ ATPase Proton
Pump Inhibitors (PPI’s)
-“Prazole’s”= more effective at suppressing acid/healing ulcers than H2 blockers
-MOA: work by inhibiting the hydrogen-potassium ATPase enzyme ,the proton pump, which is responsible for the final step in gastric acid secretion.
-Uses: Gerd, esophagitis, active duodenal ulcer, Zollinger-Ellison Syndrome
Pharm: take 30-60 mins before largest meal of day
Half life: only a few hours but duration of action is long (when initiating usually 18-24 hrs to work)
-ADE’s: Increased risk of fractures with >1 year of use, prolonged acid suppression=vitamin B 12 deficiency, supplement with ca citrate, diarrhea, C diff, low mag, increased risk of PNA
-Oral agent of Omeprazole + NaHCO3
that has a faster onset of action
-Dexilant has a dual released formula and can be taken w/o regard to meal
* Nexium, Prevacid, Protonix are IV
-Ex: Lansoprazole, Dexlansoprazole,
Omeprazole, Esomeprazole,
Pantoprazole, Rabeprazole
Prostaglandins
-Misoprostol (Cytotec) approved for the prevention of NSAID induced ulcers
MOA: PGE-1 produced by gastric mucosa, inhibits secretion of acid and stimulates secretion of mucus and HCO3 (Cytoprotective)
-Can be used prophylactially in those who take a lot of NSAID’s and are at increased risk for ulcer
-A deficiency of prostaglandins is thought to be involved in the pathology of peptic ulcers)
-CI: DO NOT USE THIS DRUG IN PREGNANCY/CHILDBEARING AGE
-ADE: Dose related diarrhea is the most common
Antacids
-Weak bases that react with gastric
acid to form water and a salt to
diminish gastric acidity
-Also decrease pepsin activity
Uses: symptomatic relief of PUD, heartburn, GERD
Pharm: Most effective AFTER meals
-Chem: Varies widely,Efficacy of an antacid depends on its capacity to neutralize gastric HCl and whether the stomach is full or empty— food delays stomach emptying, allowing more time for antacid to react and prolonging action of the medication
ADE: Aluminum hydroxide (constipation) Magnesium hydroxide (diarrhea), accumulation and ADEs can occur in those with renal disease
-Ex: Aluminum hydroxide, Aluminum hydroxide + magnesium hydroxide + simethicone, Aluminum hydroxide + magnesium hydroxide, Calcium Carbonate, Magnesium hydroxide,
Sodium bicarbonate
Mucosal Protective Agents
-MOA: have actions to enhance mucosal protection mechanisms—preventing mucosal injury, reducing
inflammation and healing ulcers
-Cytoprotective compounds
-Ex. Sucralfate, Bismuth subsalicylate (Pepto-Bismol)
Sucralfate
-Forms a complex gel with epithelial cells by creating a physical barrier that protects the ulcer from pepsin and acid, allowing the ulcer to heal
-Effective to treat duodenal ulcers and prevent stress ulcers—but use is limited due to the need for multiple daily doses, drug- drug interactions.
-It requires an acidic pH for activation—should not be given with PPIs, H2B or antacids
-Well tolerated; it can bind to other drugs and interfere with their absorption
Bismuth subsalicylate
-NAUSEA, Heartburn, indigestion, upset stomach, DIARRHEA- hey! pepto-bismol! ;)
-Used as part of quadruple therapy to treat H. Pylori
-It has antimicrobial actions—it inhibits the activity of pepsin, increases secretion of mucous and interacts with glycoproteins in necrotic mucosa to coat and protect the ulcer
What 2 sites in the brainstem play a role in vomiting?
- Chemoreceptor trigger zone [CTZ]—located outside the blood-brain barrier— can respond directly to chemical stimuli in the blood or CSF
*2. Vomiting center—located in the medulla, coordinates the motor mechanisms of vomiting; also responds to afferent input from the
vestibular system, the periphery and higher brainstem and cortical structures
Why does Chemo cause nausea/vomiting?
- Can directly activate the medullary CTZ or the vomiting center
- Dopamine receptor Type 2 and Serotonin Type 3 play major roles
- These drugs can act on the periphery by causing cell damage in the GI tract and by releasing serotonin from the cells of the small bowel.
4, Serotonin activates receptors on vagal and splanchnic afferent fibers, then send a signal to the medulla—leading to the vomiting mechanism
