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Flashcards in GI drugs I Deck (49):
1

what is the cause of ulcers

increased acidity or decreased mucosal resistance. caused or promoted by gastric acid

2

where is a peptic ulcer located

in the duodenum

3

what three receptors are present on the parietal cell in the stomach and what do they do?

gastrin, Ach, and histamine. all act to stimulate the K+/H+ ATPase.

4

what does histamine do the cell

increases the formation of cyclic AMP

5

what does gastrin and cholinergics do the parietal cell

increases intracellular calcium

6

where does gastrin come from in the stomach

the antrum

7

where does Ach come from in the stomach

from vagal input

8

where does histamine come from in the stomach

stimulated by both Ach and gastrin

9

define the mucosal protection from acid

there is a pH gradient from very low, to 7 caused by the secretion of bicarbonate. this protects the mucosa from damage. there is reduced bicarb secretion in DU patients.

10

what is the approach to treating ulcers

relief of symptoms, promotion of healing, prevention of complications, prevention of recurrence.

11

what is the treatment plan for ulcers

neutralize acid, decrease acid production, increase resistance

12

antacid therapy

only effective when they can elevate the pH to above 5. stops pepsins damage as well as acidic erosion. best if taken 1 hour after eating when gastrin activity is highest. liquids work better

13

calcium carbonate

reacts slowly with HCl to form calcium chloride and carbonic acid. it is constipating so given with magnesium compounds as laxatives

14

what are the SE of calcium carbonate

milk-alkali syndrome, nephrocalcinosis, rebound acidity, digitalis antagonism d

15

sodium bicarbonate

rarely used because of systemic alkalosis, enhanced effects of amphetamine, quinidine, cinchophen. high sodium content

16

magnesium hydroxide and carbonate

hydroxide is more potent. may cause magnesium intoxication in renal disease.

17

magnesium hydroxide and carbonate SE

diarrhea, hypokalemia, hypermagnesemia, iron deficiency

18

aluminum hydroxide

combines to form al-Cl and water. aluminum is excreted in the feces when it combines with phosphate. this is also useful in protecting the mucosa and doesnt perturb the electrolytes in the body. useful in renal patients.

19

adverse of effects of aluminum chlorides

constipation, phosphate depletion, weakness, anemia, tetany, apnea, delayed gastric emptying, concretions, fecaloma, perforation, peritonitis, encephalopathy. impaired absorption of tetracycline and digoxin.

20

what is defoaming agent and what does it do

within an antacid preparation, claims to disperse the antacid.

21

what is an adverse effect of all antacids

increases the luminal pH

22

antacids cause the decreased absorption of what

dicumarol, L-dopa

23

antacids cause the increased absorption of what

phenothiazines, INH, nalidixic acid, nitrofurantoin, pen G, sulfonamides, premature release of enteric coated tablets.

24

anticholinergics for ulcer treatment

vagotomy effect reduction of HCl secretion. spasmolytic effect.

25

adverse effects of anticholinergics

dry mouth, blurred vision, atony of the bladder, constipation, drowsiness, mental confusion.

26

when are anticholinergics contraindicated

pyloric obstruction, hiatal hernia, peptic esophagitis,

27

what are the common anticholinergics

atropine, propantheline, metantheline bromide.

28

when to administer anticholinergics

30 min before meals and at bedtime.

29

why give the anticholinergics before bed

to reduce nocturnal secretion by vagal block when antacids are not being consumed.

30

H2 blockers agents

cimetidine, ranitidine, famotidine, nizatidine

31

H2 blockers do what

lower acid secretion by blocking the receptor on parietal cells which mediates the release of acid. decreases both basal and food stimulated. can be given prophylactically to reduce stress ulcers.

32

adverse effects of H2 blockers

uncommon. HA, lethargy, confusion, depression and hallucinations.

33

what are the drug interactions for the H2 blockers

P450, theophylline, warfarin, dilatin, lidocaine.

34

H+/K+ ATPase inhibitors agents

omeprazole, lansoprazole, rabeprazole, esomeprazole, pantoprazole, dexlansoprazole.

35

general H+/K+ ATPase inhibitors

these are noncompetitive inhibitors. acitvated by acidic pH. inhibits 90% of 24 hr secretion. better pain relief and healing than the H2-blockers. will even heal H2 refractory ulcers.

36

adverse effects of the H+/K+ ATPase inhibitors

headache gynecomastia, inhibition of 450, gastric hyperplasia. not recommended for long-term use due top carcinoid tumors.

37

what drugs do the H+/K+ ATPase inhibitors interact with

warfarin, diazepam, dilantin

38

what are the agents that decrease the mucosal defenser

NSAIDs, H. pylori, smoking, genetics, stress.

39

hat drugs coat the ulcer/crater

bismuth salts (pepto), sucralfate

40

how do bismuth salts work

in acid they form crystals that precipitate on the ulcer. they have a lower ulcer recurrence rate than H2.

41

how does sucralfate work

aluminum hydroxide complex of sucrose binds to the ulcerated tissue after activation in the acid environment.

42

what are the SE of the coating agents

no adverse effects. constipation, aluminum tox, renal failure.

43

prostaglandin E2 analogs agent

misoprostol

44

misoprostol does what

decreased acid production, increase mucous and bicarbonate secretion. less effective than H2. t

45

what is misoprostol mainly used for

to prevent NSAID induced gastric ulcer

46

adverse effects of misoprostol

transient diarrhea, cannot use in pregnancy

47

drugs that eradicate H pylori

bismuth salts and antibiotics (metronidazole + tetracycline/amoxicillin

48

what is triple therapy for h pylori

a PPI/ranitidine bismuth citrate 2X/day and 2 of amoxicillin/clarithromycin/metronidazole.

49

what is quadruple therapy for h pylori

PPI 2 X
tetracycline 4 X
bismuth subsalicylate or subcitrate 4X
metronidazole 3 X.