GI drugs I Flashcards

1
Q

what is the cause of ulcers

A

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

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2
Q

where is a peptic ulcer located

A

in the duodenum

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3
Q

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

A

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

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4
Q

what does histamine do the cell

A

increases the formation of cyclic AMP

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5
Q

what does gastrin and cholinergics do the parietal cell

A

increases intracellular calcium

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6
Q

where does gastrin come from in the stomach

A

the antrum

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7
Q

where does Ach come from in the stomach

A

from vagal input

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8
Q

where does histamine come from in the stomach

A

stimulated by both Ach and gastrin

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9
Q

define the mucosal protection from acid

A

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.

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10
Q

what is the approach to treating ulcers

A

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

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11
Q

what is the treatment plan for ulcers

A

neutralize acid, decrease acid production, increase resistance

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12
Q

antacid therapy

A

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

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13
Q

calcium carbonate

A

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

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14
Q

what are the SE of calcium carbonate

A

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

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15
Q

sodium bicarbonate

A

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

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16
Q

magnesium hydroxide and carbonate

A

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

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17
Q

magnesium hydroxide and carbonate SE

A

diarrhea, hypokalemia, hypermagnesemia, iron deficiency

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18
Q

aluminum hydroxide

A

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.

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19
Q

adverse of effects of aluminum chlorides

A

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

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20
Q

what is defoaming agent and what does it do

A

within an antacid preparation, claims to disperse the antacid.

21
Q

what is an adverse effect of all antacids

A

increases the luminal pH

22
Q

antacids cause the decreased absorption of what

A

dicumarol, L-dopa

23
Q

antacids cause the increased absorption of what

A

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

24
Q

anticholinergics for ulcer treatment

A

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.