Gi: Anti-Ulcer Rx

Front 1

Most effective drugs for tx and preventing PUD

Back 1

Antimicrobials (Amox, Clarithromcin, Metronidazole, Tetracyline) bc they eradicate H. pylori

Front 2

Penicillin of choice for H. pylori

Back 2

Amoxicillin

Front 3

Macrolide of choice for H. pylor

Back 3

Clarithromycin

Front 4

Co administration of _____ with antacids (or any substance containing metal ions) significantly < antibiotic efficacy due to chelation

Back 4

Tetracycline

Front 5

Most effective agents for reducing intragastric acidity

Back 5

PPIs (irreversibly block final common pathway)

Front 6

Effectively < all forms of gastric acid secretion (esp nocturnal)

Back 6

H2 receptor blockers (TIDINE)

Front 7

Drugs of choice for Zollinger-Ellison syndrome and GERD as well as ulcer tx

Back 7

PPIs (AZOLES)

Front 8

Name 2 drugs that protect the ulcer surface

Back 8

Scralfate and Bismuth Subsalicylate

Front 9

Replaces PGs in the gastric mucosa

Back 9

Misoprostol (PGE1)

Front 10

Used to tx ulcers induced by NSAIDs

Back 10

Misoprostol

Front 11

Use of antibiotics to eliminate H. pylori may worsen this condition

Back 11

GERD (due to the removal of the buffering action of NH4 produced by the bacteria)

Front 12

Name 3 established associations with H. pylori

Back 12

PUD (gastric or duodenal); MALT lymphoma, Gastric cancer

Front 13

Ab used to treat H. pylori with the highest resistance

Back 13

Metronidazole

Front 14

Name the 2 possible combo therapies for H. pylori induced ulcers

Back 14

1. PPI + (Amox for 5 days followed by Clarithromycin + Tinidazole for 5 days): P ACT

2. PPI + Bismuth + Tetracycline + Metronidazole for 14 days: P TMB

Front 15

Which drugs cannot be given with Sucralfate and why?

Back 15

PPIs, antacids and H2 blockers should not be given with Sucralfate bc Sucralfate requires an acidic environment to be activated

Front 16

What group of drugs to you give to eradicate H. pylori?

Back 16

antimircobials

Front 17

What group of drugs do you give to block stimulation of acid secretion?

Back 17

Antimuscarinics, antihistamines

Front 18

What group of drugs do you give to block acid secretion?

Back 18

PPIs

Front 19

What group of drugs do you give to buffer acid?

Back 19

antacids

Front 20

Why is amoxicillin a better choice than ampicillin?

Back 20

Amox has better oral bioavailability

Front 21

In general, what makes Amox a good choice to tx H. pylori?

Back 21

Broad spectrum, good oral bioavailability and acid stable

Front 22

MOA of Amoxicillin

Back 22

CIDAL cell wall inhibitor (beta-lactam)

Front 23

SE of Amox

Back 23

HS

Front 24

Why is Clarithromycin a better choice than Erythromycin?

Back 24

Clarithromycin is more acid stable

Front 25

In general, why is Clarithromycin a good choice to tx H. pylori?

Back 25

Substantially lower MIC90 than azithromycin, acid stable and few side effects

Front 26

What makes Clarithromycin better than Azithromycin to tx H. pylori?

Back 26

Clarithromycin has a lower MIC50 and MIC90

Front 27

MOA of Clarithromycin

Back 27

Static protein synthesis inhibitor (50S ribosome preventing translocation)

Front 28

Special instructions when taking Tetracyline to tx H. pylori

Back 28

Take with food to < absorption, thereby increasing its actions in the lumen of the stomach; Opposite of normal instructions!

Front 29

Do NOT take Tetracylines with ______ or ______

Back 29

antacids or dairy products as it will chelate

Front 30

MOA of Tetracyline

Back 30

Static protein synthesis inhibitor (30 S to prevent addition of amino acids to growing peptide)

Front 31

SE of Tetracycline

Back 31

Photosensitivity, brown discoloration of teeth (CONTRA IN PREG!)

Front 32

MOA of Metronidazole/Tinidazole

Back 32

CIDAL;not well known, but acts as an election sink; reduction liberates toxic intermediates which damage DNA and other macromolecules

Front 33

SE of Metronidazole/Tinidazole

Back 33

Disulfiram-like, inhibits CYP2C9, CNS, GI

Front 34

What important drug does Metronidazole potentiate?

Back 34

Warfarin (> its effects!)

Front 35

What drug would potentiate the effects of Metronidazole?

Back 35

Cimetidine decreases the plasma clearance of Metronidazole

Front 36

What are the 2 distinctly different MOA of bismuth subsalicylate?

Back 36

Limited antimicrobial activity agains H. Pylori (distrupts cell wall causing lysis, prevents adhesion, inhibits urease) and protects ulcer surface (coats and stimulates PG, mucous and HCO3 secretion)

Front 37

How does Bismuth subsalicylate protect the ulcer surface?

Back 37

Stimulates PG, mucous and Bicarb secretion and also coats ulcer surface

Front 38

What drug has different actions in the stomach and LI (where it fxns as an antidiarrheal)

Back 38

Bismuth Subsalicylate (OTC)

Front 39

SE of Bismuth

Back 39

blackening of stool and tongue; high doses of bismuth subsalicylate may lead to salicylate toxicity (resp alkalosis, tinnitus, etc)

Front 40

What conditions must be met for PPIs to work?

Back 40

acidic environment and works only on active H/K ATPase (only found on the parietal cell)

Front 41

T or F: PPIs are superior to H2 antagonists or antacids in providing sx relief for heartburn

Back 41

FALSE

Front 42

AZOLE that is OTC

Back 42

Omeprazole (Priolosec)

Front 43

70% of South Pacific Islanders may be poor metabolizers of this drug.

Back 43

Omeprazole (def of CYP2C19 to activate the drug) thus, giving Esomeprazole may give a therapeutic adv

Front 44

Why must PPIs be administered in the fasting state?

Back 44

Food causes larger amplitude movements which will crush the protective coatings and expose the drugs to the stomach acid and inactivate them

Front 45

Why should you administer PPIs 1 hour before a meal?

Back 45

PPIs only inhibit active pumps and need an acidic env to work (this way, peak serum concentrations will match with max pump activity and in the fasting state, acid is lower)

Front 46

What is behind the theory of once daily dosing of PPIs?

Back 46

Irreversibly bind the to H/K ATPase which take about 18 hours to synthesize new ones. Note that PPIs still have a short t 1/2!

Front 47

Full acid inhibition is seen when with PPIs?

Back 47

only after 3-4 days of daily dosing

Front 48

Which PPIs are available IV for tx of stress-reduced ulcers?

Back 48

Esomeprazole, Lansoprazole and Pantoprazole

Front 49

Even though most SE are few, what are some possible ones of PPIs? (Short term)

Back 49

headache, diarrhea, post-therapy rebound acid hypersecretion is very common, however!

Front 50

What has been shown with long term use of PPIs

Back 50

< absorption of B12, Fe, Ca and Zn --> hip fx and > risk of respiratory and enteric infections (hospital pts can develop C diff!)

Front 51

Why can you use antimuscarinics (Atropine and Pirenzipine) to tx ulcers? (Although rarely used)

Back 51

Block ACh which stimulates M3 receptors directly on the parietal cell as well as ECL cells to release Histamine indirectly stimulating parietal cells to release H+

Front 52

Why are antimuscarinics rarely used to tx ulcers?

Back 52

Delay gastric emptying and prolong exposure of ulcer to acid; also more SE than H2 blockers

Front 53

Where are muscarinic receptors found?

Back 53

Smooth and cardiac muscle and glands (parietal cells); G protein linked-->phospholipase C and D-->increased IP3 and Ca++

Front 54

What are the anticholinergic SE?

Back 54

Anorexia, Blurry vision, Constipation, Confusion, Dry mouth, Sedation, Stasis of urine

Front 55

Name the primary and secondary effects of H2 blockers

Back 55

Primary: competitive inhibitors of parietal cell H2 receptors
Secondary: reduce intracellular cAMP inhibiting all forms of acid secretion

Front 56

Dosing for H2 blockers

Back 56

twice daily if Rx

Front 57

What is the concern with H2 blockers and the elderly?

Back 57

cleared by a combo of heaptic met, glomerular filtration and renal tubular secretion, thus < of up to 50% and reduction in volume of distribution in the elderly

Front 58

H2 blocker that undergoes little 1st pass metabolism and has a bioavailability of 100%

Back 58

Nizatidine

Front 59

Which H2 blockers are available IV for use in the tx of stress related ulcers?

Back 59

Cimetidine, Famotidine and Ranitidine

Front 60

Why do H2 blockers interact with Metronidazole?

Back 60

compete for renal tubular secretion with weak bases, increasing their actions

Front 61

All H2 blockers inhibit gastric 1st pass met of ethanol (esp women) except ______

Back 61

Famotidine

Front 62

IV infusion of H2 blockers may cause:

Back 62

Mental status changes and if rapid, bradycardia and HypOtension

Front 63

Long term use of Cimetidine may cause what?

Back 63

gynecomastia and impotence inmen and galactorrhea in women

Front 64

What effects does Cimetidine have on other dugs?

Back 64

> their effects as it inhibits CYP enzymes

Front 65

May also be used as a Ca supplement

Back 65

CaCO3 (Tums)

Front 66

How are good antacids absorbed?

Back 66

NOT absorbed systemically

Front 67

slow rate of dissolution: antacid

Back 67

Al hydroxide

Front 68

Fast rate of dissolution

Back 68

Sodium Bicarbonate (absorbed systemically --> worst SE)

Front 69

SE of Aluminum Hydroxide

Back 69

Constipation

Front 70

SE of Mg Hydroxide

Back 70

Osmotic diarrhea

Front 71

Serious (but rare) SE of Aluminum Hydroxide

Back 71

< Phosphate absoption--> Increased Ca loss--> osteomalacia

Front 72

Serious (but rare) SE of Mg Hydroxide

Back 72

renal insufficiency-->hyperMgemia-->CNS and cardio toxicity

Front 73

SE of Ca Carbonate and Na Bicarbonate

Back 73

Belching and gastric distension (produce CO2)

Front 74

Serious (but rare) SE of this drug include: mild systemic alkalosis and possible Milk-alkali syndrome

Back 74

Ca Carbonate

Front 75

Serious (but rare) SE of this drug include: severe metabolic alkalosis, alkalinizes urine, milk alkali syndrome, absoption of NaCl-->fluid retention in pts with heart/HTN/renal probs

Back 75

Na Bicarbonate

Front 76

Pt subtype where Milk alkali syndrome is observed

Back 76

Pts taking Ca carbonate for a Ca supplement

Front 77

Drug that is added to antacids that produce CO2 (Ca Carbonate and Na Bicarb); decreases surface tension decreasing gas and pain

Back 77

Simethicone

Front 78

Antacids will ____gastric absorption of weak acids

Back 78

decrease

Front 79

Antacids will ____gastric absorption of weak bases

Back 79

increase

Front 80

Antacids will ____excretion of weak acids

Back 80

increase

Front 81

Antacids will ____ excretion of weak bases

Back 81

decrease

Front 82

SE of Sucralfate

Back 82

Constipation

Front 83

MOA of Sucralfate

Back 83

sucrose sulfate Al hydrozide complex that attaches to the BM of the ulcer; NO acid neutralizing properties

Front 84

Locally blocks that actions of NSAIDs on the stomach lining, leaving the NSAIDs free to act systemically at their target site

Back 84

Misoprostol

Front 85

True or False: Misoprostol may raise gastric pH AND protect the surface

Back 85

TRUE: reduces histamine stimulated cAMP production and stimulates mucous and bicarb secretion

Front 86

SE of Misoprostol

Back 86

Stimulates uterine contractions