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Pharmacology 3 > GI Agents > Flashcards

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
Q

Why is H2 blockers a double edged sword?

A

bacterial translocation- the increase pH stimulates bacterial reproduction, which increases the risk of nosocomial pneumonia

26
Q

What do PPIs end in? Administered how?

A

“-prazole”

IV, RX, OTC

27
Q

What is significant about PPIs?

A

IRREVERSIBLE

28
Q

How does PPI work?

A

suppress acid secretion by inhibiting H/K ATPase pump on the surface of parietal cells

(inhibits the final common pathway)

29
Q

How can function return to parietal cells?

A

generate new pumps (old pump permanently damaged)

30
Q

T OR F

PPI are fast on fast off

A

FALSE

acid secretion may continue to be inhibited even after discontinuation of the medication

31
Q

What is the most potent class of acid procession inhibitors?

A

proton pump inhibitors

32
Q

What is the caution with PPIs?

A

interact with drugs that require an acidic media for absorption (itraconazole, digoxin, iron)

33
Q

How are PPIs eliminated?

A

Hepatically, so better for patients in renal insufficiency

34
Q

How does a prokinetic agent work?

A

stimulates peristalsis

35
Q

Indications for pro kinetic agents? (4)

A

1) anti-emetics
2) GERD
3) gastroparesis
4) facilitate feeding tube placement

36
Q

Where do you place a feeding tube?

A

post pyloric, this decreases reflux since the patient is supine

37
Q

Name the 2 main prokinetic drugs

A

Metoclopramide (reglan)

Cisapride

38
Q

What is metoclopramide used for?

A

enhances upper GI smooth muscle response to ACh, which results in increased GI motility and accelerated gastric emptying

39
Q

What is the other effect of metoclopramide?

A

blocks dopamine receptors in the chemo trigger zone

40
Q

What is the chemo trigger zone?

A

vomiting center in the brain, blocked by metoclopramide

41
Q

What is the a/e of metoclopramide? Caution in what patients?

A

Tremor

NOT for Parkinson’s patients

42
Q

How does Cisapride work? (4)

A

increases LES tone
increases GI motility
Acceleraties GI emptying time
Enhancing GI response to Ach at the mesenteric plexus

43
Q

What is the difference between metoclopramide & cisapride?

A

cisapride effects are seen throughout the entire GI tract and is therefore more potent

44
Q

what are 3 common A/E of pro kinetic agents?

A

diarrhea, dizziness, confusion

45
Q

What is the risk with cisapride?

A

can cause QT interval prolongation and tornadoes de points

46
Q

What is the cisapride program called?

A

Propulsid Limited Access Program, closed distribution of the drug. you must get EKG then call the supply company

47
Q

What drug interactions do you worry about with pro kinetics?

A

anticholinergics, these cause constipation which is the opposite of what you want.

48
Q

How do antacids work?

A

contain salt and neutralize acid

49
Q

Aluminum causes what?

A

Constipation

50
Q

Magnesium cause what?

A

Diarrhea

51
Q

What is an a/e of antacids?

A

cause taste disturbances

52
Q

what is the caution with antacids?

A

sodium load

chelation

53
Q

How does alginic acid work?

A

foams and blocks the lower esophagus so that acid from the stomach can not come up

54
Q

What is misoprostol?

A

Prostaglandin analogue

55
Q

What is the use of misoprostol?

A

prevention of NSAID induced ulcers

56
Q

Who should get misoprostol?

A

coprescription with patients taking ASA for arthritis

57
Q

What is the theoretical worry with misoprostol?

A

increase pain and inflammation, but not the case that is another PG family

58
Q

How does misoprostol work?

A

stimulates mucus production

59
Q

what are adverse effects of misoprostol?

A

diarreha, uterine contractions

NOT IN PREGNANT WOMEN (abortions)

Pharmacology 3 (10 decks)

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