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GI Agents Flashcards

1
Q

What are the 2 types of ulcers?

A

Gastric

Duodenal

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2
Q

Why are duodenal ulcers common?

A

First place that deals with acid from the stomach

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3
Q

Who is susceptible to stress ulcers? (4)

A

Critically ill
Mechanically ventilated for 48 hours
Head trauma
Burn trauma (trauma pts become hypermetabolic)

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4
Q

What is the bacteria that is bad for GI?

A

H. pylori

Gram negative bacteria that makes HCO3- (baking soda) shield which neutralizes the acid

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5
Q

How do NSAIDS cause ulcers? (3)

A

1) decrease gastric mucus production
2) anticoagulation
3) lower pH (acidic)

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6
Q

What occurs in Zollinger-Ellison syndrome?

A

Acid recreating pancreatic tumor

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7
Q

How do you treat ulcers?

A

increase mucous, decrease acid

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8
Q

What is GERD?

A

gastric acid backs up into the esophagus

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9
Q

GERD treatment? (4)

A

decrease acid
coat & protect esophagus
improve LES tone
lower abdominal pressure

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10
Q

what is the opposite of GERD?

A

achalasia

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11
Q

How does H pylori create an ulcer?

A

low grade inflammation, progresses to an ulcer.

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12
Q

How to prostaglandins impact the stomach?

A

stimulate mucus production

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13
Q

How does ACh impact the gut?**

A

Stimulates gut NE/Epi which decreases acid production **

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14
Q

What are the 2 stimulants of the parietal cell? What do they do?

A

Ach
Histamine
pump hydrogen (acid) into the stomach

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15
Q

What is sucralfate?

A

ulcer treatment that is not used often. it is minimally absorbed from the gut and produces a local effect so well-tolerated with minimal adverse effects.

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16
Q

how does sucralfate work?

A

band-aid protectant effect, coats the ulcers.

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17
Q

what is the problem with sucralfate?

A

may chelate some meds (binds heavy metals) and ends up in poop

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18
Q

what are 2 examples of heavy metals?

A

multivitamins, antacids

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19
Q

What is a H-2 Blocker? what do they end in?

A

“-tidine”

histamine-2 receptor blocker, which prevents parietal cells from releasing H+ into the lumen of the gut

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20
Q

Where are H-1 receptors found?

A

Periphery, causes allergic reaction

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21
Q

What are the A/E of H2 receptor blockers? (3)

A
  • CNS alterations
  • confusion
  • thrombocytopenia (decreased platelet count)
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22
Q

How are H2 blockers eliminated?

A

Renally, so dose adjustment may be required and confusion increased in low CrCl

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23
Q

What do H2 blockers interact with?

A

drugs which require an acidic media for absorption

  • itraconazole (antifungal)
  • digoxin
  • iron

since H2 blockers increase the pH in stomach and make it more basic, these drugs can not be absorbed as easily.

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24
Q

What is Vitamin C?

A

ascorbic acid, so coformulated or prescribed with iron

25
Why is H2 blockers a double edged sword?
bacterial translocation- the increase pH stimulates bacterial reproduction, which increases the risk of nosocomial pneumonia
26
What do PPIs end in? Administered how?
"-prazole" | IV, RX, OTC
27
What is significant about PPIs?
IRREVERSIBLE
28
How does PPI work?
suppress acid secretion by inhibiting H/K ATPase pump on the surface of parietal cells (inhibits the final common pathway)
29
How can function return to parietal cells?
generate new pumps (old pump permanently damaged)
30
T OR F PPI are fast on fast off
FALSE acid secretion may continue to be inhibited even after discontinuation of the medication
31
What is the most potent class of acid procession inhibitors?
proton pump inhibitors
32
What is the caution with PPIs?
interact with drugs that require an acidic media for absorption (itraconazole, digoxin, iron)
33
How are PPIs eliminated?
Hepatically, so better for patients in renal insufficiency
34
How does a prokinetic agent work?
stimulates peristalsis
35
Indications for pro kinetic agents? (4)
1) anti-emetics 2) GERD 3) gastroparesis 4) facilitate feeding tube placement
36
Where do you place a feeding tube?
post pyloric, this decreases reflux since the patient is supine
37
Name the 2 main prokinetic drugs
Metoclopramide (reglan) | Cisapride
38
What is metoclopramide used for?
enhances upper GI smooth muscle response to ACh, which results in increased GI motility and accelerated gastric emptying
39
What is the other effect of metoclopramide?
blocks dopamine receptors in the chemo trigger zone
40
What is the chemo trigger zone?
vomiting center in the brain, blocked by metoclopramide
41
What is the a/e of metoclopramide? Caution in what patients?
Tremor | NOT for Parkinson's patients
42
How does Cisapride work? (4)
increases LES tone increases GI motility Acceleraties GI emptying time Enhancing GI response to Ach at the mesenteric plexus
43
What is the difference between metoclopramide & cisapride?
cisapride effects are seen throughout the entire GI tract and is therefore more potent
44
what are 3 common A/E of pro kinetic agents?
diarrhea, dizziness, confusion
45
What is the risk with cisapride?
can cause QT interval prolongation and tornadoes de points
46
What is the cisapride program called?
Propulsid Limited Access Program, closed distribution of the drug. you must get EKG then call the supply company
47
What drug interactions do you worry about with pro kinetics?
anticholinergics, these cause constipation which is the opposite of what you want.
48
How do antacids work?
contain salt and neutralize acid
49
Aluminum causes what?
Constipation
50
Magnesium cause what?
Diarrhea
51
What is an a/e of antacids?
cause taste disturbances
52
what is the caution with antacids?
sodium load | chelation
53
How does alginic acid work?
foams and blocks the lower esophagus so that acid from the stomach can not come up
54
What is misoprostol?
Prostaglandin analogue
55
What is the use of misoprostol?
prevention of NSAID induced ulcers
56
Who should get misoprostol?
coprescription with patients taking ASA for arthritis
57
What is the theoretical worry with misoprostol?
increase pain and inflammation, but not the case that is another PG family
58
How does misoprostol work?
stimulates mucus production
59
what are adverse effects of misoprostol?
diarreha, uterine contractions NOT IN PREGNANT WOMEN (abortions)

Pharmacology 3 (10 decks)

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