GERD and PUD Tx I Flashcards
What are the Proton Pump Inhibitors
dexlansoprazole esomeprazole lansoprazole omeprazole pantoprazole rabeprazole
H2 receptor antagonists
cimetidine
famotidine
nizatidine
ranitidine
what are the antiacids
sodium bicarb
calcium carbonate
magnesium hydroxide/aluminum hydroxide
What agents provide mucosal protection
bismuth subcitrate
bismuth subsalicylate
misoprostol
sucralfate
What Antibiotics are used for Tx H.pylori
amoxicillin
clarithromycin
metronidazole
tetracycline
what NT increase acid secretion
Ach and gastrin that increase cytosolic Ca causing acid secretion from H+/K ATPase pump
When Ach and gastrin bind enterochromaffin like cells what happens
histamine is released
histamine acts where
binds H2 R on parietal cells and activates proton pump via GPCR pathways
which mediator Ach or gastrin has direct stimulation on parietal cells
Ach
What do antral D cells produce
somatostatin
what is the role of somatostatin
inhibits gastrin acid secretion
what stimulates release of somatostatin
when gastric pH falls below 3 SSt is stimulated and it suppresses gastrin
How do Prostaglandins E2 and I2 affect proton pump
reduce cAMP and thus inhibit the proton pump
how do NSAIDS contribute to ulcers
block PG prduction causing more acid secretion, less mucus and bicarb and diminished blood flow
what are various causes of GERD
transient lower esophageal sphincter relaxation, reduced lower esophageal sphincter tone, delayed gastric emptying or hormonal changes due to pregnancy
Sx GERD
heartburn, regurg and chest pain
Atypical Sx GERD
dyspepsia, epigastric pain, nauseam bloating, belchins
What are the alarm Sx of GERD
bleeding, anemia, early satieity, unexplained weight loss, progressive dysphagia, recurrent vomiting, family Hx of GI cancer, previous esophagogastric malignancy
What are lifestyle modifications for GERD
weight loss head of bed elevation avoid meals 2-3 hr before bedtime smoking cessation cessation of foods that may aggravate reflux
what are Tx options for mild intermittent GERD
antacid or H@RA as needed
what are Tx for pharmacotherapy
NERD- antacid or H@RA
what are Tx for erosive esophagitis
PPI for 8 weeks
What is PUD
mucosal damage secondary to pepsin and gastric acid occuring in stomach or proximal duodenum
causes of PUD
H pyloric infection, chronic NSAID use, stress releated mucosal injury, Zollinger Ellison Syndrome
What are Sx of PUD
burning epigastric pain, pain after meals or on empty stomach, nocturnal pain relieved by food intake
What is Tx for duodenal ulcer
H2RA or PPI for 4 weeks
what is Tx for gastric ulcer
PPI for 8 weeks
what is Tx for H pylori eradication
has been shown to reduce risk of recurrence antisecretory agent (PPI) and 2 antibiotics
MOA PPIs
inactive prodrugs that are lipophlic weak bases that diffuse readily across lipid membranes into acidified compartments from the alkaline intestinal lmen
when forms covalen disulfide bond with H/K ATPase becomes active and IRREVERSIBLY inactivates the enzyme
pharmacokinetics of PPIs making them really good drugs
short serum half lives but long duration of action at site
when should one take a PPI
on empty stomach at least 30 min before a meal
What are PPIs used to Tx
GERD, PUD and H pylori infections NSAID ulcers, prevention of re-bleeding stress related mucosal injury zollinger ellison syndrome heartburn OTC Tx
adverse effects of PPIs
diarrhea, HA and abdominal pain
increased risk of hospital and community acquired C difficile!!
decreased vit B12 absorption, increase risk hip fracture
increasesd risk nosocomial pneumonia
increased risk of enteric infections
drug interactions with PPIs
- decreased gastric pH change drug absorption like digoxin and itraconazole and atazanavir
- ompreazole may inhibit metabolis warfarin, dizepam, phenytoin and others
- could reduce clopidogrel activation reducing anti-platelet activity
what drugs should be switched from omeprazole if patients is on clopidogrel? why?
pantoprazole or rabeprazole
could decrease antiplatelet activity
What are the H2 R antagonists
cimetidine, famotidine, nizatidine and ranitidine
MOA H2RA
competitive inhibition at parietal cell H2 R
blocks histamine released form eCL cells by gastrin or vagal stimulation
what type of acid secretion do H2RA block
basal, so nocturnal acid secretion which relies on histamine instead of meal stimulated by Ach or gastrin
most important determinant of duodenal ulcer healing
control of nocturnal acid secretion
adverse effects of H2RA
diarrhea, HA fatigue, myalgia constipation
mental status changes
increased risk nosocomial pneumonia
bradycardia with rapid IV
adverse effect of cimetidine
gynecomastia or impotence in men and galactorrhea in women
drug drug interactions of H2RA
interferes with CYPs, especially cimetidine (theophylline, warfarin, phenytoin and lidocaine)
competes with creatinine and other drugs for renal tubular secretion
inhibit first pass metabolism of alcohol!!!
MOA antacids
weak bases that react with HCl to form a salt and water
neutralizes acid and reduces intragastric aciditiy
PK and effects of Na bicarb
reacts rapidly with HCl ro produce CO2 and NaCl
formation CO2 leads to distention and belching
NaCl absorption leading to fluid retention pose risk in HF and HTN paitents
PK and effects of Ca carbonate
reacts slowly with HCl for form CO2, CaCl2
may cause belching and metabolic alkalosis
hypercalcemia, renal insufficiency and metabolic alkalosis
PK and effects of Mg Hydroxide/ aluminum hydroxide
reacts slowly with HCl ro form MgCl2 or AlCl3 and H2O
no gas generated
Mg salts- osmotic diarrhea
Al salts- constipation
Uses for antacids
dyspepsia and intermittent heartburn
D-D interaction antacids
may bind and change absoprtion of other drugs
increase intragastric pH so that drug dissolution or solubility is altered
- do NOT gibe in 2 hours of tetracyclines and fluoroquinolones and Fe
final common pathway acid secretion
proton pump inhibitor
how long after taken of PPI drug will patient start secreting acid
3-4 days
