GERD and PUD Tx I Flashcards

1
Q

What are the Proton Pump Inhibitors

A
dexlansoprazole
esomeprazole
lansoprazole
omeprazole
pantoprazole
rabeprazole
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2
Q

H2 receptor antagonists

A

cimetidine
famotidine
nizatidine
ranitidine

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3
Q

what are the antiacids

A

sodium bicarb
calcium carbonate
magnesium hydroxide/aluminum hydroxide

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4
Q

What agents provide mucosal protection

A

bismuth subcitrate
bismuth subsalicylate
misoprostol
sucralfate

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5
Q

What Antibiotics are used for Tx H.pylori

A

amoxicillin
clarithromycin
metronidazole
tetracycline

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6
Q

what NT increase acid secretion

A

Ach and gastrin that increase cytosolic Ca causing acid secretion from H+/K ATPase pump

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7
Q

When Ach and gastrin bind enterochromaffin like cells what happens

A

histamine is released

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8
Q

histamine acts where

A

binds H2 R on parietal cells and activates proton pump via GPCR pathways

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9
Q

which mediator Ach or gastrin has direct stimulation on parietal cells

A

Ach

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10
Q

What do antral D cells produce

A

somatostatin

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11
Q

what is the role of somatostatin

A

inhibits gastrin acid secretion

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12
Q

what stimulates release of somatostatin

A

when gastric pH falls below 3 SSt is stimulated and it suppresses gastrin

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13
Q

How do Prostaglandins E2 and I2 affect proton pump

A

reduce cAMP and thus inhibit the proton pump

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14
Q

how do NSAIDS contribute to ulcers

A

block PG prduction causing more acid secretion, less mucus and bicarb and diminished blood flow

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15
Q

what are various causes of GERD

A

transient lower esophageal sphincter relaxation, reduced lower esophageal sphincter tone, delayed gastric emptying or hormonal changes due to pregnancy

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16
Q

Sx GERD

A

heartburn, regurg and chest pain

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17
Q

Atypical Sx GERD

A

dyspepsia, epigastric pain, nauseam bloating, belchins

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18
Q

What are the alarm Sx of GERD

A

bleeding, anemia, early satieity, unexplained weight loss, progressive dysphagia, recurrent vomiting, family Hx of GI cancer, previous esophagogastric malignancy

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19
Q

What are lifestyle modifications for GERD

A
weight loss
head of bed elevation
avoid meals 2-3 hr before bedtime
smoking cessation
cessation of foods that may aggravate reflux
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20
Q

what are Tx options for mild intermittent GERD

A

antacid or H@RA as needed

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21
Q

what are Tx for pharmacotherapy

A

NERD- antacid or H@RA

22
Q

what are Tx for erosive esophagitis

A

PPI for 8 weeks

23
Q

What is PUD

A

mucosal damage secondary to pepsin and gastric acid occuring in stomach or proximal duodenum

24
Q

causes of PUD

A

H pyloric infection, chronic NSAID use, stress releated mucosal injury, Zollinger Ellison Syndrome

25
Q

What are Sx of PUD

A

burning epigastric pain, pain after meals or on empty stomach, nocturnal pain relieved by food intake

26
Q

What is Tx for duodenal ulcer

A

H2RA or PPI for 4 weeks

27
Q

what is Tx for gastric ulcer

A

PPI for 8 weeks

28
Q

what is Tx for H pylori eradication

A
has been shown to reduce risk of recurrence
antisecretory agent (PPI) and 2 antibiotics
29
Q

MOA PPIs

A

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

30
Q

pharmacokinetics of PPIs making them really good drugs

A

short serum half lives but long duration of action at site

31
Q

when should one take a PPI

A

on empty stomach at least 30 min before a meal

32
Q

What are PPIs used to Tx

A
GERD, PUD and H pylori infections
NSAID ulcers, prevention of re-bleeding
stress related mucosal injury
zollinger ellison syndrome
heartburn OTC Tx
33
Q

adverse effects of PPIs

A

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

34
Q

drug interactions with PPIs

A
  • 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
35
Q

what drugs should be switched from omeprazole if patients is on clopidogrel? why?

A

pantoprazole or rabeprazole

could decrease antiplatelet activity

36
Q

What are the H2 R antagonists

A

cimetidine, famotidine, nizatidine and ranitidine

37
Q

MOA H2RA

A

competitive inhibition at parietal cell H2 R

blocks histamine released form eCL cells by gastrin or vagal stimulation

38
Q

what type of acid secretion do H2RA block

A

basal, so nocturnal acid secretion which relies on histamine instead of meal stimulated by Ach or gastrin

39
Q

most important determinant of duodenal ulcer healing

A

control of nocturnal acid secretion

40
Q

adverse effects of H2RA

A

diarrhea, HA fatigue, myalgia constipation
mental status changes
increased risk nosocomial pneumonia
bradycardia with rapid IV

41
Q

adverse effect of cimetidine

A

gynecomastia or impotence in men and galactorrhea in women

42
Q

drug drug interactions of H2RA

A

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!!!

43
Q

MOA antacids

A

weak bases that react with HCl to form a salt and water

neutralizes acid and reduces intragastric aciditiy

44
Q

PK and effects of Na bicarb

A

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

45
Q

PK and effects of Ca carbonate

A

reacts slowly with HCl for form CO2, CaCl2
may cause belching and metabolic alkalosis
hypercalcemia, renal insufficiency and metabolic alkalosis

46
Q

PK and effects of Mg Hydroxide/ aluminum hydroxide

A

reacts slowly with HCl ro form MgCl2 or AlCl3 and H2O
no gas generated
Mg salts- osmotic diarrhea
Al salts- constipation

47
Q

Uses for antacids

A

dyspepsia and intermittent heartburn

48
Q

D-D interaction antacids

A

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

49
Q

final common pathway acid secretion

A

proton pump inhibitor

50
Q

how long after taken of PPI drug will patient start secreting acid

A

3-4 days