Dyspepsia and GERD Flashcards
What is dyspepsia? What are 3 subclassifications? What are some causes?
INDIGESTION
Postprandial fullness (termed postprandial distress syndrome)
Early satiation (meaning inability to finish a normal sized meal or postprandial fullness)
Epigastric pain or burning (termed epigastric pain syndrome)
Causes of Dyspepsia o Food intolerances o Medication intolerance o PUD/GERD o Malignancy o Pancreatic/biliary disorders o Systemic diseases (CAD, thyroid, adrenal) o Functional dyspepsia (~50%) Delayed gastric emptying Impaired gastric accomodation Hypersensitivity to gastric distention Genetic factors Role of H.pylori Post-infectious association Psychosocial factors
What is the diagnostic approach to dyspepsia?
o History and physical examination
o Presence of alarm symptoms
o Diagnostic options:
Diagnostic EGD with evaluation for h.pylori
Test and treat for h.pylori
Empiric antisecretory therapy
What are some treatment options for dyspepsia?
Treatment Options
o Acid suppression
o Eradication of infection
o Prokinetic agents
o Antidepressants/neuromodulating agents
o Psychologic interventions
What is the classic presentation of GERD? What are some atypical presentations?
Heartburn
– Retrosternal burning discomfort, radiating toward the neck, and most commonly experienced after meals.
Regurgitation
– Effortless return of gastric or esophageal contents into the pharynx without nausea, retching, or abdominal contractions. Patients typically regurgitate acidic material mixed with small amounts of undigested food.
Dysphagia
– Difficulty swallowing solids or liquids
ATYPICAL Pulmonary: Asthma Chronic bronchitis Asp pneumonia
Non-cardiac chest pain
Sleep disturbances
Dental Erosions
ENT: Cough Sore throat Hoarseness Laryngitis Post nasal drainage
How is the classic GERD diagnosed? Atypical?
Classic + relief to therapy
- heartburn
- regurgitation
- exacerbation by meals
- worse when recumbent
- nocturnal symptoms
ATYPICAL
May require: 24 hour ambulatory pH monitor (Bravo), upper endoscopy, manometry
List various etiologies of GERD.
Impaired acid neutralization by saliva and HCO3
Impaired esophageal motility
Lower Esophageal Sphincter
(weak LES or inappropriate relaxation)
Hiatal hernia
Delayed gastric emptying/gastroparesis
Describe various lifestyle modifications to treat GERD.
Elevating Head of Bed
Dietary Modification
– Small Volume Meals
– Low-fat
– Avoid chocolate, peppermint, coffee, carminatives (onion, garlic),
Avoid Recumbency for Three Hours After Eating
Avoiding Medications (Calcium channel blockers, theophyline, nitrates) that affect LES Pressure or Damage the Esophagus
Weight loss
Stop smoking, ETOH, caffeine, citrus/acidic foods
What are the treatment goals for GERD pharmacology?
Gastric pharmacology—treatment goals
Prevent symptoms: pain, dyspepsia
Prevent mucosal injury
Prevent bleeding
Prevent cancer
Alter motility
Describe the physiology of gastric secretion including the roles of histamine, ACh, prostaglandins, and gastrin? What modulates these things? What pathways do the secretions use to lead to acid and/or mucous secretion and/or inhibition?
ACh uses a Ca+ dependent pathway to cause the HK atpase to release acid. Gastrin does the same. Histamine uses a camp dependent pathway to do the same. Prostaglandins block that camp pathway. Prostaglandings also cause epithelial cells to secrete mucous and bicarb. NSAIDs/aspirin block prostaglandin synth. Gastrin and ACh cause histamine to be secreted by ECL cells.
What are some examples of antacids? What do they do? What are their advantages? What are their side effects? Which shouldn’t be used? Why?
Magnesium hydroxide
Aluminum hydroxide
Balanced mixtures of each used most commonly (Mylanta, Maalox)
Calcium bicarbonate (TUMS) and sodium bicarbonate (baking soda)
They neutralize acid in the stomach.
Quick onset of action
Short duration of action
Inexpensive
Side effects of antacids:
– Mg(OH)2 – DIARRHEA, elevated Mg levels in renal failure
– Al(OH)3 – CONSTIPATION, elevated aluminum levels in renal failure
– Combinations – diarrhea can still be a problem, but better
– Ca(HCO3)2 – BELCHING, nausea, abdominal distention from CO2 release, increased calcium Levels, alklalosis, calcium may cause rebound acid
– NaHCO3 – BELCHING alkalosis, sodium load (cardiac and renal patients)
– Alkaseltzer – (Aspirin/NaHCO3/citric acid) Aspirin component: irrational choice for patients Predisposed to peptic ulcer disease
– All: altered absorption of other drugs because alter gastric and urinary pH (osteoporosis, encephalopathy, myopathy)
What are two types of cytoprotective agents? What do they do? What is their mechanism? What are their side effects? When are they indicated?
–Sucrose-octasulfate: sucralfate (Carafate)
–Major mechanism is coating of mucosa
–Need to take frequently (four times daily = qid)
–Highest dose = 4 grams daily—can cause constipation
-Altered drug absorption (take other drugs at least 2 hours before)
-Caution in renal failure
–Prostaglandin derivatives: misoprostil (Cytotec)
–Side effects—diarrhea, sponteneous abortion
–Expensive
–Often used with NSAIDS to prevent erosions and ulcers
What is the mechanism of H2RAs? When do they work best? What are the side effects? What are some examples? Which one has some extra side effects? What are they?
Block histamine receptor at gastric parietal cell and ECL cell
Structures all similar to histamine
Pharmacology of H2-receptor antagonists
4 oral, 3 IV forms available
Best at suppressing nocturnal acid production
H2RA reach the parietal cell through the blood
Little protein binding in the blood
Adjust doses for renal failure (cut dose in half)
Few side effects
VERY WELL TOLERATED
Rare thrombocytopenia
Cimetidine, Ranitidine, Famotidine, Nizatidine
Cimetidine: inhibits estradiol metabolism with long-term use:
Gynecomastia/Galactorrhea
Diminished sperm count/impotence
P450 inhibition alters metabolism of other drugs
How is it activated? What is its mechanism? How do they reach their target location? Side effects? Examples?
–Rapidly activated by acid
–Must be protected from gastric acid by a coating
–Absorbed quickly into blood
–Short circulating half-life (1 hr)
–Covalently bind proton pump in parietal cell
–Long biological half-life (that of the proton pump)
–5 oral, 3 IV forms
–Suppress acid production by 80-95%
–Takes several doses to have full effect (70% inhibited at steady state)
–PPIs reach the parietal cell through the blood
–Few side effects
VERY WELL TOLERATED
(i) Omeprazole (Prilosec, Rapinex, Zegerid)
(ii) Esomeprazole (Nexium)
(iii) Lansoprazole (Prevacid, Dexilant)
(iv) Rabeprazole (Aciphex)
(v) Pantoprazole (Protonix)
