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PHARM: PUD and GI Disorders Flashcards

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1
Q

What is the role of surface epithelial cells in the stomach?

A

protection: make mucous and bicarbonate

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2
Q

What is the role of parietal cells in the stomach?

A

secrete HCl to bring the pH of hte stomach to below 1 (needed to convert pepsinogen to pepsin)

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3
Q

What are the most powerful stimulators of the neurotransmitters that stimulate parietal cells?

A

Vagus Nerve
Food
Protein

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4
Q

The vagus nerve releases _____ to stimulate _____ to make _____ which stimulates the parietal cells to release HCl.

A

The vagus nerve releases ACETYLCHOLINE to stimulate G CELLS to make GASTRIN which stimulates the parietal cells to release HCl

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5
Q

Other than G Cells, which cells are stimulated by the vagus nerve?

A

ECL cells (release histamine to also regulate HCl secretion by parietal cells)

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6
Q

What type of parietal cell receptors do gastrin and Ach act on?

A

Gq receptors

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7
Q

What type of parietal cell receptors does Histamine act on?

A

Gs receptors

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8
Q

What type of parietal cell receptors do somatostatins and prostaglandins act on?

A

Gi receptors

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9
Q

What do both Gq and Gs receptors cause?

A

drive the H+/K+ ATPase and send H+ out into lumen

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10
Q

What condition is cause by normal or reduced gastric acid output with altered mucosal resistance (or low bicarbonate) leading to damage?

A

Gastric ulcers

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11
Q

What condition is caused by high gastric acid output (especially at night) with inadequate duodenal bicarbonate secretion and insufficient acid neutralization?

A

Duodenal ulcers

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12
Q

What condition is caused by insufficient constriction of the esophageal sphincter, resulting in exposure of esophagus to gastric acids?

A

GERD

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13
Q

List the 3 drugs that work to increase protective mechanisms of the stomach.

A

Bismuth Subsalicylate
Sucralfate
Misoprostol

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14
Q

What is Bismuth Subsalicylate?

A

Pepto Bismol

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15
Q

MOA: stimulates mucus and HCO3- production (at super-therapeutic doses)

A

Misoprostol

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16
Q

MOA: enhances secretion of mucus and HCO3-, weakly inhibits pepsin activity, chelates with proteins at the base of the ulcer crater and forms protective barrier against acid and pepsin, and inhibits H. Pylori

A

Bismuth Subsalicylate

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17
Q

MOA: forms sticky, viscous gel that adheres to gastric epithelial cells protecting them from acid and pepsin

A

Sucralfate

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18
Q

Which cytoprotective agent requires an acidic pH to act?

A

Sucralfate

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19
Q

Which cytoprotective agent is an analog of PGE1?

A

Misoprostol

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20
Q

Which cytoprotective agent is used in PPI induced pneumonia and PUD?

A

sucralfate

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21
Q

Which cytoprotective agent is rarely used, and only really used in patients who must use NSAIDs?

A

Misoprostol

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22
Q

Which cytoprotective agent gives intolerable diarrhea in 40% of patients?

A

Misoprostol

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23
Q

Which macrolide is used to eradicate H. Pylori?

A

Clarithromycin

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24
Q

Which beta-lactam is used to eradicate H. pylori?

A

Amoxicillin

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25
Which antibiotic is used to eradicate H. pylori in patients with allergies to penicillin?
tetracycline
26
Which antibiotic has high likelihood of resistance so is ALWAYS used in combinations?
metronidazole
27
What type of bugs does metronidazole selectively kill?
obligate anaerobes
28
What is the name of the Nitrofuran antibacterial and antiprotozoal used to kill H. pylori?
furazolidine
29
What is tritec? Why is it not commonly used anymore?
Ranitidine, Bismuth and Clarithromycin | H2 blockers are not as effective as PPIs in triple therapy
30
What is Helidac?
Pepto-Bismol, metronidazole, tetracycline
31
What is the quadruple regimen used in quadruple therapy for H. pylori eradication?
omeprazole, Pepto-Bismol, clarithromycin, metrondiazole
32
When do patients with GERD regurgitate food?
night (when stomach is full)
33
What are the 2 things that must occur to lead to a reflux episode?
* GI contents must be ready to reflux | * Anti-reflux mechanism at LES is compromised
34
True or false: Peptic Ulcer Disease is typically NOT caused by NSAIDs or hyperacidity/stress
TRUE
35
What is implicated as the underlying cause of 92% of duodenal ulcers and 70% of gastric ulcers?
H. pylori infection
36
How do you diagnose H. pylori infection?
blood antibody or urea breath tests.
37
MOA: neutralize gastric acid in the stomach (NaHCO3 + HCl → NaCl + CO2 +H2O)
Antacids
38
MOA: Bind to and block H2 receptor stimulation by histamine (competitive antagonists)
H2 blockers
39
MOA: delivered to parietal cells to diffuse into the secretory canaliculi where it gets trapped by the proton pump due to acidic pH (and becomes protonated) and irreversibly inhibits the H+ ion pump
PPIs
40
Why are antacids not used as sole therapy for things like PUD?
CANNOT prevent transformation of pepsinogen to pepsin (would need pH >4)
41
When do H2 blockers work best?
inhibit mostly basal and nocturnal gastric secretion (volume and H+ concentration)
42
Can pepsin be formed with H2 blocker therapy?
YES, only slight change in pH occurs
43
What are the indications for H2 blockers?
- Rarely used for PUD - Used for mild symptoms of GERD - Prevent stress-related upper GI bleeds in seriously ill patients (rarely)
44
What is unique about PPIs pharmacokinetics?
Have enteric coating that releases drug into intestine (absorbed into blood where it can return and SPECIFICALLY inhibit parietal cells)
45
List the 2 types of non-systemic antacids.
Aluminum Hydroxides | Magnesium Hydroxides
46
List the types of systemic antacids.
Calcium or Sodium Bicarbonate
47
List the antiflatulant used to decrease gas tension.
Simethicon
48
What is the most potent H2 antagonist.
Famotidine
49
What is the least potent H2 antagonist.
Cimetidine
50
What is the PPI with the least CYP450 metabolism?
Rabeprazole
51
What antacid gives constipation?
aluminum hydroxides
52
What antacid gives diarrhea?
Magnesium hydroxides
53
What antacids can lead to acid reflux and fluid retention?
calicum or sodium bicarbonate
54
What must you be mindful of when taking antacids?
do NOT take these within 1-2 hours of other drugs (significantly alters absorption)
55
Which antacid class is for SHORT TERM USE ONLY?
systemic (calcium or sodium bicarbonate)
56
When should you take antacids?
1hr and 3hr after a meal and at bedtime
57
List some examples of behavioral therapies for GERD.
* Decrease gastric contents (decrease meal size, no food after 7pm) * Weight reduction (stops abdomen from pushing on stomach) * Head of bed elevation (food not pushed up against esophagus in supine position) * Avoid agents that decrease LES tone: fat, coffee, peppermint
58
What is the role of prokinetics in GERD treatment?
increase gastric motility (improve LES tone and competence to enhance esophageal clearance and improve gastric emptying)
59
List the prokinetics.
Metoclopramide Domperidone Cisapride (not in US unless special permission)
60
MOA: Dopaminergic neuron secretes dopamine to inhibit firing of post-synaptic motor neurons and prevent Ach release from causing constriction of SM in LES
Metoclopramide and Domperidone
61
MOA: NANC targeted by 5-HT4 (positive regulator, releases Ach on post-synaptic motor neuron to cause contraction of SM in LES)
Cisapride
62
What is the major difference between Metoclopramide/Domperidone MOA and Cisapride MOA?
Metoclopramide/Domperidone constrict LES and increase gastric emptying while Cisapride only works to contract LES
63
What is the major adverse effect seen with Metoclopramide?
tardive dyskinesia (only give drug 1-2 weeks at a time, because if you get this, it is IRREVERSIBLE)

GI (21 decks)

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