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Upper GI Pharm Flashcards

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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
When do we see maximum gastric acid suppresion?
2-5 days bc not all cells are active at same time
26
What is the best tx for IMMEDIATE acid suppresion?
parenterally with Esomeprazole, | Pantoprazole, or Lansoprazole,
27
Metabolism of PPIs?
via hepatic CYPS | may interfere with the elimination of other drugs cleared by this route
28
Side effects of PPIs
nausea, abdominal pain, constipation, flatulence, and diarrhea. Chronic use: bone fracture and more susceptible to some infections
29
_______is more frequent and more severe | with proton pump inhibitors than with H2 receptor antagonists
Hypergastrinemia
30
Uses of PPIs
gastric and duodenal ulcers and to treat gastroesophageal reflux disease (GERD) and heartburn Mainstay for hypersecretory conditions, including the Zollinger-Ellison syndrome.
31
Cimentidine and Ranitidine are examples of
H2 antagonists
32
Mechanism of Cimentidine and Ranitidine:
competitve (reversible) H2 receptor inhibition on parietal cells
33
What is more potent, H2 antagonists or PPIs
PPI but H2 can still suppress 24 hr gastric acid secreation by 70% thus GREAT at suppressing nocturnal acid secreation
34
Why are H2 antagonists a good tx for duodenal ulcers?
most important determinant of duodenal ulcer healing is the level of nocturnal acidity, evening dosing of H2 -receptor antagonists may be adequate
35
How are H2 antagonists metabolized?
kidneys, thus need to use reduced doses of H2 antagonists in pts with low creatinine clearance
36
Side effects of H2 antagonistsI
IG well tolerated;occastionally see diarrhea, headache, drowsiness, fatigue, muscular pain, and constipation
37
Whats concerning with Cimentidine>
H2 antagonists tat inhibits CYPs and can increase the levels of a variety of drugs that are substratesfor these enzymes
38
Uses of H2 antagonsits
gastric and duodenal ulcers, uncomplicated GERD, and to prevent the occurrence of stress ulcers
39
What happens overtime when we use H2 antagonists?
tolerance, even w/in 3 days; This could be due | to a secondary hypergastrinemia that stimulates ECL cell histamine release
40
potent inhibitors of acid secretion made by gastric mucosa
PGE2 and PGI2
41
prevent gastric injury by stimulating mucin and bicarbonate secretion and increasing mucosal blood flow.
PGE2, PGI2
42
What blocks PGE2 and PGI2 production in gastric mucosa?
NSAIDS and aspirin; thus predisposes pts to ulcers
43
= octasulfate of sucrose + Al(OH)3
Sucralfate
44
MOA of Sucralfate
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
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
Sucralfate
46
When would you presecribe Sucralfate
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
side effects of sucralfate
Constipation and inhibits absorption of drugs
48
Mechanism of antacids
neutralizes HCl
49
Side effect of CO2 containing antacids
Release of CO2 from bicarbonate- and carbonate-containing antacids can cause belching, nausea, abdominal distention, and flatulence
50
Side of Ca++ containing antacid
may induce rebound acid secretion
51
Side effect of Al3+ containing antacid
Al3+ relaxes the gastric smooth muscle, producing delayed gastric emptying and constipation
52
concern with Mg+ containing antacid
Mg causes diarrhea
53
What do we need to be careful of when using antacids?
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
____ and ___ containing antacids are notable for their ability to chelate drugs in the GI tract, forming insoluble complexes that pass without absorption
Mg2+ and Al3+
55
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
~30 minutes. 2-3
56
used as an antidiarrheal for treating travelers’ diarrhea. It has antimicrobial, anti-inflammatory, anti-secretatory actions and is sometimes used to treat ulcers.
Bismuth subsalicylate
57
How does bismuth subsalicylate work
bismuth compounds bind to the base of the ulcer, promote mucin and bicarbonate production, and have significant antibacterial effects.
58
What antibiotics are used to tx H.pylori?
Metronidazole, Clarithromycin, Amoxicillin, Tetracycline
59
What do we use in combination with antibiotics when treating H.pylori?
Bismuth subsalicylate, K+/H+ ATPase or H2 blockers for 10-14 days!!!
60
_______prevents NSAID-induced ulcers by prostaglandin replacement. Contraindicated in pregnant women or those contemplating pregnancy.
Misoprostol
61
antacids used to neutralize secreated acid
Al(OH)3, CaCO3, Mg(OH)2)
62
____ can cause diarrhea and is cautioned in patients with renal insufficiency.
Mg(OH)2
63
____ can cause constipation.
Al(OH)3
64
Forms a polymer gel to coat stomach lining and | protect it.
Sucralfate – octasulfate of sucrose plus Al(OH)3.
65
What do we need to be aware of with Cimetidine?
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
methyl PGE1 derivative used to prevent DNSAID induced mucosal injury. Abortificient and exacerbate IBD.
Misoprostol
67
antacid that is rapidly cleard, short duration with an alkali and sodium load
NaHCO3; not really used bc you are giving pt an alkali load and sodium load thus not good for pts with heart issues
68
a surfactnant that is a common additive to antacids to decrease gas or break up bubbles
simethicone
69
What do we need to keep in mind when doing antibiotic treatements for H.pylori
1 antibiotic is NOT enough!!! need more then 1 for 10-14 days and pts MUST be compliant to erradicate bug
70
Tx for active ulcer d/t H.pylori
reduce acid AND eradicate H.pylori
71
Tx for NSAID related ulcer
reduce acid and replace prostaglandins
72
Tx for ulcer not d/t H.pylori or NSAID use
reduce acid

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