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Upper GI Pharm Flashcards

1
Q

Gastric acid secretion:
Acid is produced by gastric
parietal cells and transported to
lumen via _____ (the proton pump).

A

H+/K+ ATPase

exchanges hydrogen and potassium ions across the parietal cell membrane

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2
Q

This pump generates the
largest ion gradient known in
vertebrates, with an intracellular pH of ~7.3 and an intracanalicular pH of ~0.8.

A

H+/K+ ATPase

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3
Q

Enterochromaffin-like (ECL) cells, the source of gastric_____, usually are in close proximity
to parietal cells.

A

histamine

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4
Q

Histamine acts as a paracrine mediator, diffusing from its site of release to nearby parietal cells, where it activates ____receptors.

A

H2

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5
Q

H2 receptors are____ and activate the Gs–adenylyl cyclase-cyclic AMP-PKA pathway

A

GPCRs

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6
Q

_____which is produced by antral G cells, is the most potent inducer of acid secretion.

A

Gastrin

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7
Q

Gastrinstimulates acid secretion indirectly by inducing the release of_____ by ECL cells; a direct effect on parietal cells also a lesser role.

A

histamine

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8
Q

Gastrin activates GPCRs (cholecystokinin receptors, CCK2) that couple to the _________pathway in parietal cells.

A

Gq–PLC-IP3–Ca2+

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9
Q

Acetylcholine release from postganglionic vagal fibers stimulates gastric acid secretion through _______receptors on the basolateral membrane of parietal cells.

A

muscarinic M3

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10
Q

_____increases

the release of histamine from the ECL cells and of gastrin from antral G cells

A

Acetylcholine

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11
Q

Somatostatin (SST), produced by antral D cells, inhibits

A

gastric acid secretion.

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12
Q

Acidification of the gastric luminal pH to <3 stimulates_____ release, which in turn suppresses gastrin release.

A

SST or somatostatin release

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13
Q

Why do pts with H.pylori have excess gastrin production?

A

SST-producing cells are decreased in patients with H. pylori infection, and the consequent reduction of SST’s inhibitory effect may contribute to excess gastrin production.

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14
Q

A key defense against ulcer formation is the secretion of a mucus layer that helps protect the gastric epithelia. This layer traps secreted_____ at the cell surface

A

bicarbonate

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15
Q

Gastric mucus is soluble when
secreted but quickly forms an insoluble gel that coats the mucosal surface of the stomach and prevents mucosal damage by______.

A

pepsin

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16
Q

Role of prostaglandins E2 and I2

A

Mucus production is stimulated by prostaglandins E2 and I2, which also directly inhibit gastric acid secretion by parietal cells.

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17
Q

How do NSAIDS affect mucous layer in stomach?

A

Inhibition of prostaglandin formation (NSAIDs, ethanol) decreases mucus secretion and predisposes the patient to the development of acid-peptic disease

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18
Q

H+/K+ ATPASE INHIBITORS are what kind of therapies?

A

Gastric acid lowering
Omeprazole
Esomeprazole
Lansoprazole

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19
Q

key feature of proton pump inhibitors?

A

prodrugs

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20
Q

Once PPIs are absorbed, where do they go?

A

diffuse into gastric parietal cells, accumulate in acidic secreatory canaliculi

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21
Q

what happens in the caniliculi to the PPIs

A

activated by catalized formation of sulfonamide that cant diffuse back thus its trapped in parietal cell

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22
Q

How do PPIs inactivate the H+/K+ pump?

A

sulfonamide covalently binds w/ cystein sulfhydryl groups in the pump and irreversible inactive the pump

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23
Q

How long does the PPI have effect, what is teh half life?

A

lasts 24-48 hours bc new pump needs to be made and 1/2 is only .5 to 2 hrs

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24
Q

How do we prevent degredation of PPI in gastric lumen?

A

oral forms that are enteric coated or powdered omeprazole + sodium bicarbonate

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25
Q

When do we see maximum gastric acid suppresion?

A

2-5 days bc not all cells are active at same time

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26
Q

What is the best tx for IMMEDIATE acid suppresion?

A

parenterally with Esomeprazole,

Pantoprazole, or Lansoprazole,

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27
Q

Metabolism of PPIs?

A

via hepatic CYPS

may interfere with the elimination of other drugs cleared by this route

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28
Q

Side effects of PPIs

A

nausea, abdominal pain, constipation, flatulence, and diarrhea.
Chronic use: bone fracture and more susceptible to some infections

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29
Q

_______is more frequent and more severe

with proton pump inhibitors than with H2 receptor antagonists

A

Hypergastrinemia

30
Q

Uses of PPIs

A

gastric and duodenal ulcers and to treat gastroesophageal reflux
disease (GERD) and heartburn
Mainstay for hypersecretory conditions, including the Zollinger-Ellison syndrome.

31
Q

Cimentidine and Ranitidine are examples of

A

H2 antagonists

32
Q

Mechanism of Cimentidine and Ranitidine:

A

competitve (reversible) H2 receptor inhibition on parietal cells

33
Q

What is more potent, H2 antagonists or PPIs

A

PPI but H2 can still suppress 24 hr gastric acid secreation by 70% thus GREAT at suppressing nocturnal acid secreation

34
Q

Why are H2 antagonists a good tx for duodenal ulcers?

A

most important determinant of
duodenal ulcer healing is the level of nocturnal acidity,
evening dosing of H2 -receptor antagonists may be
adequate

35
Q

How are H2 antagonists metabolized?

A

kidneys, thus need to use reduced doses of H2 antagonists in pts with low creatinine clearance

36
Q

Side effects of H2 antagonistsI

A

IG well tolerated;occastionally see diarrhea, headache, drowsiness, fatigue, muscular
pain, and constipation

37
Q

Whats concerning with Cimentidine>

A

H2 antagonists tat inhibits CYPs and can increase the levels of a variety of drugs that are substratesfor these enzymes

38
Q

Uses of H2 antagonsits

A

gastric and duodenal ulcers,
uncomplicated GERD, and to prevent the occurrence of
stress ulcers

39
Q

What happens overtime when we use H2 antagonists?

A

tolerance, even w/in 3 days; This could be due

to a secondary hypergastrinemia that stimulates ECL cell histamine release

40
Q

potent inhibitors of acid secretion made by gastric mucosa

A

PGE2 and PGI2

41
Q

prevent gastric injury by stimulating mucin and bicarbonate secretion and increasing mucosal blood flow.

A

PGE2, PGI2

42
Q

What blocks PGE2 and PGI2 production in gastric mucosa?

A

NSAIDS and aspirin; thus predisposes pts to ulcers

43
Q

= octasulfate of sucrose + Al(OH)3

A

Sucralfate

44
Q

MOA of Sucralfate

A

undergoes extensive cross-linking, makes sticky polymer to stick to epi cells and ulcers for 6 hrs. Inhibits hydrolysis of mucosal proteins by pepsin. Cytoprotective; stims production of prostaglandins and epidermal GFs

45
Q

undergoes extensive cross-linking, makes sticky polymer to stick to epi cells and ulcers for 6 hrs. Inhibits hydrolysis of mucosal proteins by pepsin. Cytoprotective; stims production of prostaglandins and epidermal GFs

A

Sucralfate

46
Q

When would you presecribe Sucralfate

A

Peptic acid disease
may be usefull in critically ill pts to prevent stress ulcers as gastric pH may be a factor in devo of nonsocial pneumonia

47
Q

side effects of sucralfate

A

Constipation and inhibits absorption of drugs

48
Q

Mechanism of antacids

A

neutralizes HCl

49
Q

Side effect of CO2 containing antacids

A

Release of CO2 from bicarbonate- and carbonate-containing antacids can cause
belching, nausea, abdominal distention, and flatulence

50
Q

Side of Ca++ containing antacid

A

may induce rebound acid secretion

51
Q

Side effect of Al3+ containing antacid

A

Al3+ relaxes the gastric smooth muscle, producing delayed gastric emptying and
constipation

52
Q

concern with Mg+ containing antacid

A

Mg causes diarrhea

53
Q

What do we need to be careful of when using antacids?

A

By altering gastric and urinary pH, antacids can the absorption and secretion of a number of drugs (e.g., thyroid hormones, allopurinol, and imidazole antifungals),
by altering rates of dissolution and absorption, bioavailability, and renal elimination.

54
Q

____ and ___ containing antacids are notable for their ability to chelate drugs in the GI tract, forming insoluble complexes that pass without absorption

A

Mg2+ and Al3+

55
Q

Antacids are cleared from the empty stomach in ______
The presence of food is sufficient to elevate gastric pH to ~5 for 1 hour and to prolong the neutralizing effects of antacids for ____ hours

A

~30 minutes.

2-3

56
Q

used as an antidiarrheal for treating travelers’ diarrhea. It has antimicrobial, anti-inflammatory, anti-secretatory actions and is sometimes used to treat ulcers.

A

Bismuth subsalicylate

57
Q

How does bismuth subsalicylate work

A

bismuth compounds bind to the base of the ulcer, promote mucin and bicarbonate production, and have significant antibacterial effects.

58
Q

What antibiotics are used to tx H.pylori?

A

Metronidazole, Clarithromycin, Amoxicillin, Tetracycline

59
Q

What do we use in combination with antibiotics when treating H.pylori?

A

Bismuth subsalicylate, K+/H+ ATPase or H2 blockers for 10-14 days!!!

60
Q

_______prevents NSAID-induced ulcers by prostaglandin replacement. Contraindicated in
pregnant women or those contemplating pregnancy.

A

Misoprostol

61
Q

antacids used to neutralize secreated acid

A

Al(OH)3, CaCO3, Mg(OH)2)

62
Q

____ can cause diarrhea and is cautioned in patients with renal insufficiency.

A

Mg(OH)2

63
Q

____ can cause constipation.

A

Al(OH)3

64
Q

Forms a polymer gel to coat stomach lining and

protect it.

A

Sucralfate – octasulfate of sucrose plus Al(OH)3.

65
Q

What do we need to be aware of with Cimetidine?

A

It will inhibit Cytochrome P450 thus need to be aware that an affect absorption of other drugs
stuff like Rimetidine may be better especially if pt is on another drug

66
Q

methyl PGE1 derivative used to prevent DNSAID induced mucosal injury. Abortificient and exacerbate IBD.

A

Misoprostol

67
Q

antacid that is rapidly cleard, short duration with an alkali and sodium load

A

NaHCO3; not really used bc you are giving pt an alkali load and sodium load thus not good for pts with heart issues

68
Q

a surfactnant that is a common additive to antacids to decrease gas or break up bubbles

A

simethicone

69
Q

What do we need to keep in mind when doing antibiotic treatements for H.pylori

A

1 antibiotic is NOT enough!!! need more then 1 for 10-14 days and pts MUST be compliant to erradicate bug

70
Q

Tx for active ulcer d/t H.pylori

A

reduce acid AND eradicate H.pylori

71
Q

Tx for NSAID related ulcer

A

reduce acid and replace prostaglandins

72
Q

Tx for ulcer not d/t H.pylori or NSAID use

A

reduce acid

GI (14 decks)

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